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1
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Mazumder NR, Junna S, Sharma P. The Diagnosis and Non-pharmacological Management of Acute Kidney Injury in Patients with Cirrhosis. Clin Gastroenterol Hepatol 2023; 21:S11-S19. [PMID: 37625862 DOI: 10.1016/j.cgh.2023.04.033] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/07/2023] [Revised: 03/01/2023] [Accepted: 04/06/2023] [Indexed: 08/27/2023]
Abstract
Acute kidney injury in patients with cirrhosis is quite common, and is seen in up to 50% of patients hospitalized for decompensated cirrhosis. Causes of acute kidney injury include prerenal, renal, or postrenal etiologies. The diagnosis and early institution of nonpharmacologic and pharmacologic management are key to the recovery of renal function. The objective of this review is to provide a practical approach to the use of diagnostic biomarkers and highlight the nonpharmacologic management and prevention of acute kidney injury.
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Affiliation(s)
- Nikhilesh R Mazumder
- Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, Michigan; Gastroenterology Section, VA Ann Arbor Healthcare System, Ann Arbor, Michigan
| | - Shilpa Junna
- Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, Michigan
| | - Pratima Sharma
- Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, Michigan; Gastroenterology Section, VA Ann Arbor Healthcare System, Ann Arbor, Michigan.
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2
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Tota M, Baron V, Musial K, Derrough B, Konieczny A, Krajewska M, Turkmen K, Kusztal M. Secondary IgA Nephropathy and IgA-Associated Nephropathy: A Systematic Review of Case Reports. J Clin Med 2023; 12:jcm12072726. [PMID: 37048809 PMCID: PMC10094848 DOI: 10.3390/jcm12072726] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/18/2023] [Revised: 03/20/2023] [Accepted: 03/29/2023] [Indexed: 04/08/2023] Open
Abstract
Primary (pIgAN), secondary IgA nephropathy (sIgAN), and IgA-associated nephropathy can be distinguished. While pIgAN has been thoroughly studied, information about the etiology of sIgAN remains scarce. As concerns sIgAN, several studies suggest that different etiologic factors play a role and ultimately lead to a pathophysiologic process similar to that of pIgAN. In this article, we review a vast number of cases in order to determine the novel putative underlying diseases of sIgAN. Moreover, updates on the common pathophysiology of primary disorders and sIgAN are presented. We identified liver, gastrointestinal, oncological, dermatological, autoimmune, and respiratory diseases, as well as infectious, iatrogenic, and environmental factors, as triggers of sIgAN. As novel biological therapies for listed underlying diseases emerge, we suggest implementing drug-induced sIgAN as a new significant category. Clinicians should acknowledge the possibility of sIgAN progression in patients treated with TNF-α inhibitors, IL-12/IL-23-inhibitors, immune checkpoint inhibitors, CTLA-4, oral anticoagulants, thioureylene derivatives, and anti-vascular endothelial growth factor drugs.
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Affiliation(s)
- Maciej Tota
- Faculty of Medicine, Wroclaw Medical University, 50-367 Wrocław, Poland
| | - Vanessa Baron
- Faculty of Medicine, Wroclaw Medical University, 50-367 Wrocław, Poland
- Faculty of Dentistry, Wroclaw Medical University, 50-435 Wrocław, Poland
| | - Katie Musial
- Faculty of Medicine, Wroclaw Medical University, 50-367 Wrocław, Poland
| | - Bouchra Derrough
- Faculty of Medicine, Wroclaw Medical University, 50-367 Wrocław, Poland
| | - Andrzej Konieczny
- Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, 50-556 Wrocław, Poland
| | - Magdalena Krajewska
- Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, 50-556 Wrocław, Poland
| | - Kultigin Turkmen
- Division of Nephrology, Department of Internal Medicine, Meram Medical Faculty, Necmettin Erbakan University, Konya 42090, Turkey
| | - Mariusz Kusztal
- Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, 50-556 Wrocław, Poland
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3
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Wilde B, Canbay A, Katsounas A. Clinical and pathophysiological understanding of the hepatorenal syndrome: Still wrong or still not exactly right? World J Clin Cases 2023; 11:1261-1266. [PMID: 36926126 PMCID: PMC10013104 DOI: 10.12998/wjcc.v11.i6.1261] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/16/2022] [Revised: 12/15/2022] [Accepted: 02/03/2023] [Indexed: 02/23/2023] Open
Abstract
The hepatorenal syndrome (HRS) is one major extrahepatic complication of end-stage liver diseases. While circulatory dysregulation is considered as primary etiology for HRS, cirrhosis-related (systemic) inflammation and/or cardial dysfunction may also play a key pathogenic role in HRS development. Exclusion of other causes of acute kidney injury (AKI) is required for diagnosis of HRS-AKI by the definition of the International Club of Ascites. However, the pathophysiology of HRS is not understood completely and there are still limited therapeutic options. Reversibility of renal dysfunction after liver transplantation indicates that HRS-AKI is a functional disorder caused by altered cellular function. The interplay between systemic inflammation and the onset of kidney-related hypometabolism may have a key role and needs to be studied in depth. This minireview challenges simplified views of the HRS in the context of diagnostics and therapy stressing the need for further evidence to advance the knowledge on this syndrome.
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Affiliation(s)
- Benjamin Wilde
- Department of Nephrology, University of Duisburg-Essen, University Hospital Essen, Essen 45147, Germany
| | - Ali Canbay
- Department of Medicine, Ruhr University Bochum, Bochum 44892, Germany
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Abstract
AKI is commonly encountered in patients with decompensated cirrhosis, and it is associated with unfavorable outcomes. Among factors specific to cirrhosis, hepatorenal syndrome type 1, also referred to as hepatorenal syndrome-AKI, is the most salient and unique etiology. Patients with cirrhosis are vulnerable to traditional causes of AKI, such as prerenal azotemia, acute tubular injury, and acute interstitial nephritis. In addition, other less common etiologies of AKI specifically related to chronic liver disease should be considered, including abdominal compartment syndrome, cardiorenal processes linked to cirrhotic cardiomyopathy and portopulmonary hypertension, and cholemic nephropathy. Furthermore, certain types of GN can cause AKI in cirrhosis, such as IgA nephropathy or viral hepatitis related. Therefore, a comprehensive diagnostic approach is needed to evaluate patients with cirrhosis presenting with AKI. Management should be tailored to the specific underlying etiology. Albumin-based volume resuscitation is recommended in prerenal AKI. Acute tubular injury and acute interstitial nephritis are managed with supportive care, withdrawal of the offending agent, and, potentially, corticosteroids in acute interstitial nephritis. Short of liver transplantation, vasoconstrictor therapy is the primary treatment for hepatorenal syndrome type 1. Timing of initiation of vasoconstrictors, the rise in mean arterial pressure, and the degree of cholestasis are among the factors that determine vasoconstrictor responsiveness. Large-volume paracentesis and diuretics are indicated to relieve intra-abdominal hypertension and renal vein congestion. Direct-acting antivirals with or without immunosuppression are used to treat hepatitis B/C-associated GN. In summary, AKI in cirrhosis requires careful consideration of multiple potentially pathogenic factors and the implementation of targeted therapeutic interventions.
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Affiliation(s)
- Giuseppe Cullaro
- Department of Medicine, University of California, San Francisco, California
| | - Swetha Rani Kanduri
- Department of Nephrology, Ochsner Health, New Orleans, Louisiana
- Ochsner Clinical School, The University of Queensland, Brisbane, Queensland, Australia
| | - Juan Carlos Q. Velez
- Department of Nephrology, Ochsner Health, New Orleans, Louisiana
- Ochsner Clinical School, The University of Queensland, Brisbane, Queensland, Australia
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5
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Sharma P, Airy M. Glomerular Disease in Liver Disease. Clin Liver Dis 2022; 26:203-212. [PMID: 35487605 DOI: 10.1016/j.cld.2022.01.007] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Glomerular diseases are an important cause of kidney disease in patients with liver disease. Although kidney involvement due to tubular or vascular disease is more common, glomerular diseases became more prevalent as hepatitis infections increased and then subsequently decreased with the widespread availability of hepatitis A and B vaccines and the development of effective antiviral treatments for hepatitis B and C. In this review, we discuss the common glomerular pathologies that are seen in patients with liver disease and the current treatment options available to them.
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Affiliation(s)
- Purva Sharma
- Division of Kidney Disease and Hypertension, The Glomerular Disease Center at Northwell Health Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, 100 Community Drive, 2nd floor, Great Neck, NY 11021, USA.
| | - Medha Airy
- Selzman Kidney Institute, Baylor College of Medicine, 7200 Cambridge Street, 8th Floor Suite 8B, Houston, TX 77030, USA. https://twitter.com/@NephDr
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Grosser DS, Persad P, Talento RV, Shoemaker LR, Hunley TE, Hidalgo G, Subtirelu MM, Coventry S, Baliga R, Fogo AB. IgA-dominant infection-associated glomerulonephritis in the pediatric population. Pediatr Nephrol 2022; 37:593-600. [PMID: 34453602 DOI: 10.1007/s00467-021-05245-y] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/09/2021] [Revised: 06/29/2021] [Accepted: 07/12/2021] [Indexed: 11/25/2022]
Abstract
BACKGROUND IgA-dominant infection-associated glomerulonephritis is well-documented in adults but has not been studied in depth in children. We assessed the incidence of pediatric IgA-dominant infection-associated glomerulonephritis and clinical and kidney biopsy findings. METHODS Pediatric native kidney biopsies over a 10-year period with IgA dominance, strong C3, and findings indicative of infection-associated etiology were identified. RESULTS We identified 9 cases of IgA-dominant infection-associated glomerulonephritis, 0.8% of pediatric native kidney biopsies. Seven patients presented with elevated creatinine. All had hematuria and proteinuria. Eight patients had clinical evidence of infection: one each with central port infection by methicillin-sensitive Staphylococcus aureus, recurrent streptococcal pharyngitis and recent otitis media, streptococcal pharyngitis demonstrated 8 months after biopsy, suspected streptococcal scalded skin syndrome, and viral gastroenteritis, and three with serologic evidence of Streptococcal infection but no identified site of infection. All but one patient experienced short-term normalization of creatinine and resolution of proteinuria, though two eventually progressed to kidney failure: one 3 years later due to progressive disease and one 11 years later due to focal segmental glomerulosclerosis without concurrent immune deposits. CONCLUSIONS Pediatric IgA-dominant infection-associated glomerulonephritis is rare, and generally has a favorable prognosis, contrasting that seen in adults with severe comorbidities. A higher resolution version of the Graphical abstract is available as Supplementary.
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Affiliation(s)
- Daniel S Grosser
- Department of Pathology and Laboratory Medicine, University of Texas Health Science Center At San Antonio, San Antonio, TX, USA.
| | - Paul Persad
- Laboratory for Kidney Pathology, Nashville, TN, USA
| | | | - Lawrence R Shoemaker
- Department of Pediatrics, Division of Pediatric Nephrology, University of Florida College of Medicine, Gainesville, FL, USA
| | - Tracy E Hunley
- Division of Pediatric Nephrology, Monroe Carell Jr Children's Hospital At Vanderbilt, Nashville, TN, USA
| | - Guillermo Hidalgo
- Pediatric Nephrology, East Carolina University, Greenville, NC, USA
- Pediatric Nephrology, Hackensack Meridian Health, Neptune, NJ, USA
| | - Mihail M Subtirelu
- Pediatric Nephrology and Hypertension, East Tennessee Children's Hospital, Knoxville, TN, USA
| | - Susan Coventry
- Department of Pathology, Norton Children's Hospital, Louisville, KY, USA
| | | | - Agnes B Fogo
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA
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7
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A Donor With Green Kidneys—To Transplant or Not to Transplant: A Case Report. Transplant Direct 2021. [DOI: 10.1097/txd.0000000000001198] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022] Open
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Abstract
The understanding of the pathogenesis of any disease is the key to effective and specific treatment of the disease. immunoglobulin A (IgA) nephropathy is an autoimmune disease of the kidney. Oxford MEST classification is commonly used to stratify patients according to the severity of the disease. Patients with IgA nephropathy seem to produce anti-GalNAc antibodies against a particularly defective IgA1. This immune complex deposits in the kidneys, leading to a type 3 hypersensitivity reaction which ultimately damages the kidneys. People of a certain genetic background and who experience upregulation of certain defective receptors seem to develop primary IgA nephropathy. Secondary IgA nephropathy could be due to dysbiosis of the microbiota in the gut, compromised gut immunity or other gut pathologies, pulmonary function abnormalities, or amyloidosis. Overproduction of IgA due to plasma cell dyscrasia or reduced clearance of IgA due to liver abnormalities could also be potential causes. Genes that predispose individuals to IgA nephropathy and intestinal abnormalities, such as Celiac disease, seem to overlap and these people tend to have a poorer prognosis and need to be placed on more intensive treatment regimens. IgA Vasculitis seems to be a systemic form of IgA nephropathy, whereby IgA deposits systemically and leads to multiple disease manifestations. Patients in high-risk groups could also be prophylactically screened for the disease and closely monitored by immunohistochemical methods such as an enzyme-linked immunosorbent assay (ELISA) or identified by genetic testing. Currently, the major treatment regimens involve supportive therapy or immunosuppressive therapy which has major side effects. More specific treatment methods such as monoclonal antibodies, immunoglobulin replacement therapy, or low-antigen-content diet could also be looked into as potential treatment options. Stem cell replacement, by way of bone marrow transplant and tonsillectomy, has been suggested as a treatment option in patients with indications.
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Affiliation(s)
- Jemima C Stanley
- Pathology, Zhejiang University School of Medicine, Hangzhou, CHN
| | - Hong Deng
- Pathology, Zhejiang University School of Medicine, Hangzhou, CHN
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9
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Miyazaki S, Hattori A, Kuno Y, Ikeda T. IgA nephropathy with diffuse alveolar haemorrhage. BMJ Case Rep 2018; 11:11/1/e227382. [PMID: 30580306 DOI: 10.1136/bcr-2018-227382] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022] Open
Abstract
Immunoglobulin (Ig)A nephropathy is the most common cause of primary glomerulonephritis worldwide. While IgA nephropathy has been associated with a variety of other diseases, pulmonary complications are extremely rare. A 58-year-old man presented with a 2-week history of fever and exertional dyspnoea. A chest imaging revealed bilateral consolidation predominantly in upper lungs. Laboratory findings showed elevated serum creatinine with proteinuria and haematuria. Flexible bronchoscopy revealed diffuse alveolar haemorrhage, and IgA nephropathy was confirmed on a renal biopsy. He received prednisone with good effect. This case highlights the need to consider IgA nephropathy in the differential diagnosis of pulmonary renal syndrome.
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Affiliation(s)
- Shinichi Miyazaki
- Department of Pulmonary Medicine, Yokkaichi Municipal Hospital, Yokkaichi, Japan
| | - Akiko Hattori
- Department of Nephrology, Yokkaichi Municipal Hospital, Yokkaichi, Japan
| | - Yasumasa Kuno
- Department of Pulmonary Medicine, Yokkaichi Municipal Hospital, Yokkaichi, Japan
| | - Takuya Ikeda
- Department of Pulmonary Medicine, Yokkaichi Municipal Hospital, Yokkaichi, Japan
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10
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Dvanajscak Z, Karl BE, Sanchez AP, Walavalkar V. IgA-Dominant Glomerulopathy and Thrombotic Microangiopathy After Chemotherapy. Kidney Int Rep 2018; 3:492-497. [PMID: 29725655 PMCID: PMC5932117 DOI: 10.1016/j.ekir.2017.10.011] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022] Open
Affiliation(s)
- Zeljko Dvanajscak
- Department of Pathology, University of California San Diego Health, San Diego, California, USA
| | - Bethany E Karl
- Department of Nephrology, University of California San Diego Health, San Diego, California, USA
| | - Amber P Sanchez
- Department of Nephrology, University of California San Diego Health, San Diego, California, USA
| | - Vighnesh Walavalkar
- Department of Pathology, University of California San Francisco, San Francisco, California, USA
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11
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Hemminger J, Arole V, Ayoub I, Brodsky SV, Nadasdy T, Satoskar AA. Acute glomerulonephritis with large confluent IgA-dominant deposits associated with liver cirrhosis. PLoS One 2018; 13:e0193274. [PMID: 29634718 PMCID: PMC5892865 DOI: 10.1371/journal.pone.0193274] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2017] [Accepted: 02/07/2018] [Indexed: 11/18/2022] Open
Abstract
BACKGROUND Small glomerular IgA deposits have been reported in patients with liver cirrhosis, mainly as an incidental finding in autopsy studies. We recently encountered nine cirrhotic patients who presented with acute proliferative glomerulonephritis with unusually large, exuberant glomerular immune complex deposits, in the absence of systemic lupus erythematosus (SLE) or monoclonal gammopathy-related kidney disease. Deposits were typically IgA dominant/codominant. Our aim was to further elucidate the etiology, diagnostic pitfalls, and clinical outcomes. METHODS We present clinical features and kidney biopsy findings of nine cirrhotic patients with an unusual acute immune complex glomerulonephritis. We also identified native kidney biopsies from all patients with liver cirrhosis at our institution over a 13-year period (January 2004 to December 2016) to evaluate presence of glomerular IgA deposits in them (n = 118). RESULTS Six of nine cirrhotic patients with the large immune deposits had a recent/concurrent acute bacterial infection, prompting a diagnosis of infection-associated glomerulonephritis and treatment with antibiotics. In the remaining three patients, no infection was identified and corticosteroids were initiated. Three of nine patients recovered kidney function (one recovered kidney function after liver transplant); three patients developed chronic kidney disease but remained off dialysis; two patients became dialysis-dependent and one patient developed sepsis and expired shortly after biopsy. Within the total cohort of 118 patients with cirrhosis, 67 others also showed IgA deposits, albeit small; and 42 patients had no IgA deposits. CONCLUSIONS These cases provide support to the theory that liver dysfunction may compromise clearance of circulating immune complexes, enabling deposition in the kidney. At least in a subset of cirrhotic patients, a superimposed bacterial infection may serve as a "second-hit" and lead to acute glomerulonephritis with exuberant immune complex deposits. Therefore, a trial of antibiotics is recommended and caution is advised before immunosuppressive treatment is offered. Unfortunately, most of these patients have advanced liver failure; therefore both diagnosis and management remain a challenge.
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Affiliation(s)
- Jessica Hemminger
- Department of Pathology, Division of Renal and Transplant Pathology, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Vidya Arole
- Department of Pathology, Division of Renal and Transplant Pathology, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Isabelle Ayoub
- Department of Internal Medicine, Division of Nephrology, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Sergey V. Brodsky
- Department of Pathology, Division of Renal and Transplant Pathology, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Tibor Nadasdy
- Department of Pathology, Division of Renal and Transplant Pathology, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Anjali A. Satoskar
- Department of Pathology, Division of Renal and Transplant Pathology, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
- * E-mail:
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12
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An Attempt to Establish a Common Animal Model for Hepatorenal Fibrosis in Rats. PATHOLOGY RESEARCH INTERNATIONAL 2017; 2017:8260508. [PMID: 28835866 PMCID: PMC5556604 DOI: 10.1155/2017/8260508] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 02/22/2017] [Revised: 06/07/2017] [Accepted: 06/12/2017] [Indexed: 01/15/2023]
Abstract
It is already a proven fact that there exists a relationship between CLD (chronic liver disease) and kidney disease but still there is no available combined animal model of liver and kidney fibrosis on the same animal. An animal model is one of the important research tools in the field of medical science because it is important to build a model that can simulate the disease condition so that the particular disease can be studied. Therefore, the aim of this study is to build a less expensive, less time consuming, and reproducible model of hepatorenal fibrosis on rats. We administered combined intraperitoneal injection of CCl4 (Carbon Tetrachloride) and BSA (Bovine Serum Albumin) on a female Wistar rats. At the end, the liver and kidney tissues were examined under microscope to see whether we were successful in establishing the model or not. The results show that liver fibrosis was marked but the changes on the kidneys were mild. In this study, we were able to induce significant fibrosis in the liver and early stages of fibrosis in the kidneys. The result also demonstrated that the addition of BSA conferred a liver protective effect against CCl4 induced hepatotoxicity, whereas combination of CCl4 and BSA proved to be detrimental for kidneys.
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13
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Renal Outcomes in Patients With IgA Nephropathy Undergoing Liver Transplant: A Retrospective Cohort Study. Transplant Direct 2017; 3:e193. [PMID: 28795144 PMCID: PMC5540631 DOI: 10.1097/txd.0000000000000708] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/29/2017] [Accepted: 06/09/2017] [Indexed: 01/09/2023] Open
Abstract
Background End-stage liver disease (ESLD) is the most common cause of secondary immunoglobulin A nephropathy (IgAN). Multiple mechanisms have been proposed to explain the association between liver disease and IgAN. Although some mechanisms are expected to reverse in patients after liver transplant, the long-term renal prognosis is unclear for these patients. Methods This observational retrospective cohort study examined the renal outcomes of 14 patients who had IgAN with end-stage liver disease and subsequently underwent either liver transplant alone or combined liver and kidney transplant at a single tertiary care center. Results Of the 7 patients who underwent liver transplant alone, hematuria persisted in 2, 4 had progressive loss of kidney function with worsening proteinuria in 3 but only 1 reached end-stage renal disease 5 years posttransplant. Among 7 combined liver and kidney transplant recipients, 1 had histologic and 1 had histologic and clinical recurrence of IgAN without kidney allograft loss. Conclusions IgAN in patients with advanced liver disease does not necessarily resolve after liver transplant but has overall favorable renal outcomes.
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Arora A, Porwal Y, Malik R, Lall B. Secondary IgA Nephropathy presenting as nephrotic syndrome with acute renal failure in a case of alcoholic liver cirrhosis. INDIAN JOURNAL OF MEDICAL SPECIALITIES 2017. [DOI: 10.1016/j.injms.2017.04.001] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/01/2022]
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15
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Shimamura Y, Akimoto T, Moniwa N, Hasegawa K, Ogawa Y, Takizawa H. Hereditary Spherocytosis Presenting with Immunoglobulin A Nephropathy in Post-Splenectomy. J Gen Fam Med 2016. [DOI: 10.14442/jgfm.17.4_307] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/03/2022] Open
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16
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Sise ME, Wisocky J, Rosales IA, Chute D, Holmes JA, Corapi KM, Babitt JL, Tangren JS, Hashemi N, Lundquist AL, Williams WW, Mount DB, Andersson KL, Rennke HG, Smith RN, Colvin R, Thadhani RI, Chung RT. Lupus-like Immune Complex-mediated Glomerulonephritis in Patients with Hepatitis C Virus Infection Treated with Oral, Interferon-free, Direct-acting Antiviral Therapy. Kidney Int Rep 2016; 1:135-143. [PMID: 27990496 PMCID: PMC5155703 DOI: 10.1016/j.ekir.2016.06.006] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/21/2023] Open
Affiliation(s)
- Meghan E Sise
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Jessica Wisocky
- Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Ivy A Rosales
- Department of Pathology, Massachusetts General Hospital, Boston, MA
| | - Donald Chute
- Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Jacinta A Holmes
- Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Kristin M Corapi
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Jodie L Babitt
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Jessica S Tangren
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Nikroo Hashemi
- Department of Gastroenterology and Hepatology, Brigham and Women's Hospital, Boston, MA
| | - Andrew L Lundquist
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Winfred W Williams
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - David B Mount
- Renal Unit, Brigham and Women's Hospital, Boston, MA
| | - Karin L Andersson
- Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Helmut G Rennke
- Department of Pathology, Brigham and Women's Hospital, Boston, MA
| | - R Neal Smith
- Department of Pathology, Massachusetts General Hospital, Boston, MA
| | - Robert Colvin
- Department of Pathology, Massachusetts General Hospital, Boston, MA
| | - Ravi I Thadhani
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA
| | - Raymond T Chung
- Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA
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17
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Abstract
Kidney injury is associated with increased morbidity and mortality in liver transplant recipients. Since the introduction of the model for end-stage liver disease for the allocation of organs for liver transplantation in 2002, the heavy weighting of serum creatinine in the model for end-stage liver disease score has significantly increased the incidence of renal dysfunction seen among patients undergoing liver transplantation. As a result, the frequency of simultaneous liver-kidney (SLK) transplantation compared to liver transplantation alone (LTA) has also increased. The decision to perform SLK rather than LTA is an important one because the benefits to the liver transplant recipient receiving a kidney transplant must be balanced with the benefits of using that organ for a patient with end-stage renal disease. However, predicting whether or not a patient with liver failure has reversible kidney disease, and therefore does not also need a kidney transplant, is difficult. The severity and duration of pretransplant renal dysfunction, hepatitis c, diabetes, and other risk factors for kidney disease are associated with an increased risk of posttransplant end-stage renal disease. However, there are currently no clinical findings that accurately predict renal recovery post liver transplant. As a result, the rate of SLK versus LTA differs significantly between transplant centers. To increase consistency across centers, multiple guidelines have been proposed to guide the decision between SLK and LTA, but their poor predictive value has limited their uniform adoption. Nevertheless, adoption of uniform rules for the allocation of kidneys would reduce the variability between centers in rates of SLK transplant.
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18
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Sampaio MS, Martin P, Bunnapradist S. Renal dysfunction in end-stage liver disease and post-liver transplant. Clin Liver Dis 2014; 18:543-60. [PMID: 25017075 DOI: 10.1016/j.cld.2014.05.003] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Renal dysfunction is a frequent complication in patients with end-stage liver disease awaiting orthotopic liver transplantation and in the post-liver transplant period. Although the stereotypical form of renal dysfunction is the hepatorenal syndrome, other causes of acute kidney injury in this population include prerenal azotemia and acute tubular necrosis. Renal injury in a patient with cirrhosis is associated with a poor prognosis.
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Affiliation(s)
- Marcelo S Sampaio
- Division of Nephrology, Department of Medicine, Kidney and Pancreas Transplant Program, David Geffen School of Medicine at UCLA, 1015 Gayley Avenue, Suite 220, Los Angeles, CA 90024, USA
| | - Paul Martin
- Division of Hepatology, Miller School of Medicine, University of Miami, 1500 NW 12 Avenue, Jackson Medical Tower E-1101, Miami, FL 33136, USA
| | - Suphamai Bunnapradist
- Division of Nephrology, Department of Medicine, Kidney and Pancreas Transplant Program, David Geffen School of Medicine at UCLA, 1015 Gayley Avenue, Suite 220, Los Angeles, CA 90024, USA.
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19
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Ozkurt S, Acikalin MF, Temiz G, Akay OM, Soydan M. Renal hemosiderosis and rapidly progressive glomerulonephritis associated with primary hemochromatosis. Ren Fail 2014; 36:814-6. [PMID: 24588645 DOI: 10.3109/0886022x.2014.892391] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
Abstract
Hereditary hemochromatosis leads to the accumulation of iron in many organs including the liver, spleen and heart and results in injury and dysfunction of these organs. On the other hand, iron accumulation and functional impairment in kidney is extremely rare. We report a 61-year-old male patient with hereditary hemochromatosis, in whom the renal function was deteriorated rapidly. Renal biopsy revealed crescentic glomeruli and hemosiderin accumulation in tubular epithelial cells.
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Affiliation(s)
- Sultan Ozkurt
- Department of Nephrology, Faculty of Medicine, Eskisehir Osmangazi University , Eskisehir , Turkey
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20
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Minimal change disease and IgA deposition: separate entities or common pathophysiology? Case Rep Nephrol 2014; 2013:268401. [PMID: 24527245 PMCID: PMC3914242 DOI: 10.1155/2013/268401] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2013] [Accepted: 05/04/2013] [Indexed: 11/23/2022] Open
Abstract
Introduction. Minimal Change Disease (MCD) is the most common cause of nephrotic syndrome in children, while IgA nephropathy is the most common cause of glomerulonephritis worldwide. MCD is responsive to glucocorticoids, while the role of steroids in IgA nephropathy remains unclear. We describe a case of two distinct clinical and pathological findings, raising the question of whether MCD and IgA nephropathy are separate entities or if there is a common pathophysiology. Case Report. A 19-year old man with no medical history presented to the Emergency Department with a 20-day history of anasarca and frothy urine, BUN 68 mg/dL, Cr 2.3 mg/dL, urinalysis 3+ RBCs, 3+ protein, and urine protein : creatinine ratio 6.4. Renal biopsy revealed hypertrophic podocytes on light microscopy, podocyte foot process effacement on electron microscopy, and immunofluorescent mesangial staining for IgA. The patient was started on prednisone and exhibited dramatic improvement. Discussion. MCD typically has an overwhelming improvement with glucocorticoids, while the resolution of IgA nephropathy is rare. Our patient presented with MCD with the uncharacteristic finding of hematuria. Given the improvement with glucocorticoids, we raise the question of whether there is a shared pathophysiologic component of these two distinct clinical diseases that represents a clinical variant.
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21
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Abstract
GOAL To determine the risk of future biopsy-verified IgA nephropathy (IgAN) among individuals with biopsy-verified celiac disease (CD). BACKGROUND Individuals with CD suffer increased risk of end-stage renal disease. An association between CD and IgAN has been suggested; however, results have been inconclusive and no previous study has considered the risk of IgAN in biopsy-verified CD. STUDY We performed a population-based prospective cohort study. We identified 27,160 individuals with CD (Marsh stage III) and no previous renal disease through small-intestinal biopsy reports obtained between July 1969 and February 2008 in all (n=28) Swedish pathology departments. Individuals with IgAN were identified by biopsy reports acquired at the 4 Swedish pathology departments specialized in renal pathology. Cox regression analysis was used to determine the risk of future IgAN among individuals with CD compared with 133,949 age-matched and sex-matched reference individuals. RESULTS Seven (0.026%) individuals with CD and 11 (0.008%) reference individuals developed IgAN. We found an increased risk of biopsy-verified IgAN among individuals with CD [hazard ratio, 3.03; 95% confidence interval, 1.22-7.56]. The risk increase remained statistically significant after adjustment for prior liver disease and country of birth. CONCLUSIONS Individuals with CD suffer a 3-fold increased risk of future IgAN. Our findings warrant awareness of renal function in individuals with CD.
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22
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Nayak SL, Maiwall R, Nandwani A, Ramanarayanan S, Mathur RP, Kumar R, Sarin SK, Vashishtha C. Management of acute kidney injury in cirrhosis. Hepatol Int 2013; 7:813-819. [PMID: 26201918 DOI: 10.1007/s12072-013-9456-x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/25/2013] [Accepted: 06/29/2013] [Indexed: 01/15/2023]
Abstract
Acute kidney injury (AKI) is a relatively frequent problem, occurring in approximately 20 % of hospitalized patients with cirrhosis. Although serum creatinine (S Cr) is the most commonly used method to determine AKI because of easy availability and low cost, practically it underestimates the extent of kidney injury in patients with chronic liver disease. AKI is defined as an abrupt rise in S Cr of 0.3 mg/dl or more (>26.4 mmol/l) or an increase of 150 % or more (1.5-fold) from baseline. The cause of AKI in cirrhosis is multifactorial and is unique in terms of pathogenesis. The most common causes of AKI in cirrhosis can be subdivided into either functional or structural. The functional group includes volume-responsive (prerenal azotemia) and volume-unresponsive states (hepatorenal syndrome). Volume responsive is the most common type of AKI due to frequent use of diuretics, large volume abdominal paracentesis and gastrointestinal bleeding in patients with liver disease. The structural causes include acute tubular necrosis, tubulointerstitial and glomerular diseases. Patients with decompensated cirrhosis are in a vasodilatory state leading to a decrease in effective arterial blood volume, predisposing to AKI. Therefore, management of AKI depends on the underlying cause, and therapy should be directed toward removal of the cause. The outcome in cirrhosis when patients are on dialysis is very dismal. Every effort should be made to prevent AKI.
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Affiliation(s)
- Suman Lata Nayak
- Department of Nephrology, Institute of Liver & Biliary Sciences (ILBS), D-1, Vasant Kunj, New Delhi, 110070, India.
| | - Rakhi Maiwall
- Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi, India
| | - Ashish Nandwani
- Department of Nephrology, Institute of Liver & Biliary Sciences (ILBS), D-1, Vasant Kunj, New Delhi, 110070, India
| | | | - R P Mathur
- Department of Nephrology, Institute of Liver & Biliary Sciences (ILBS), D-1, Vasant Kunj, New Delhi, 110070, India
| | - Ramesh Kumar
- Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi, India
| | - S K Sarin
- Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi, India
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23
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Slack AJ, McPhail MJW, Ostermann M, Bruce M, Sherwood R, Musto R, Dew T, Auzinger G, Bernal W, O'Grady J, Heneghan MA, Moore K, Wendon JA. Predicting the development of acute kidney injury in liver cirrhosis--an analysis of glomerular filtration rate, proteinuria and kidney injury biomarkers. Aliment Pharmacol Ther 2013; 37:989-97. [PMID: 23577724 PMCID: PMC3761189 DOI: 10.1111/apt.12299] [Citation(s) in RCA: 36] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/22/2012] [Revised: 01/15/2013] [Accepted: 03/12/2013] [Indexed: 12/13/2022]
Abstract
BACKGROUND The timely diagnosis of acute kidney injury (AKI) in liver cirrhosis is challenging. AIM To evaluate whether quantification of glomerular filtration rate (GFR), proteinuria and kidney injury biomarkers can accurately predict the development of AKI. METHODS A prospective cohort analysis of patients with cirrhosis was performed. Measures of baseline kidney function included serum creatinine, iohexol clearance and urine protein:creatinine ratio. Blood and urine samples were collected daily. A retrospective analysis of cystatin C GFR and neutrophil gelatinase-associated lipocalin (NGAL) measured 48 h prior to the diagnosis of AKI was undertaken to evaluate their ability to predict the development of AKI. RESULTS Eighteen of the 34 cirrhosis patients studied developed AKI. A GFR <60 mL/min/1.73 m(2) was identified in 56% with Iohexol clearance compared to 8% using the four-variable modified diet in renal disease formula (P < 0.0001). Prediction of AKI, 48 h prior to the development of AKI with cystatin C GFR and serum NGAL concentration were similar; area under the receiver operating curve (AUROC) values 0.74 (0.51-0.97), P = 0.04 and 0.72 (0.52-0.92), P = 0.02 respectively. The development of AKI was strongly predicted by urine protein:creatinine ratio above the cut-off of >30 (equivalent to 300 mg/day of proteinuria) sensitivity 82% (57-96) and specificity 80% (52-96), AUROC 0.86 (0.73-0.98), P ≤ 0.0001. [OR 21 (3-133), P ≤ 0.002]. CONCLUSIONS In patients with liver cirrhosis a urine protein:creatinine ratio >30 predicts AKI. Iohexol clearance and cystatin C formulae identify a greater proportion of patients with a GFR <60 mL/min/1.73 m(2), which also predicts the development of AKI.
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Affiliation(s)
- A J Slack
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - M J W McPhail
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK,Hepatology and Gastroenterology, Division of Diabetes Endocrinology and Metabolism, St Mary's Hospital Campus, Imperial College LondonLondon, UK
| | - M Ostermann
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - M Bruce
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - R Sherwood
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - R Musto
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - T Dew
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - G Auzinger
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - W Bernal
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - J O'Grady
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - M A Heneghan
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
| | - K Moore
- Hepatology, Royal Free HospitalLondon, UK
| | - J A Wendon
- Institute of Liver Studies, King's College Hospital Foundation TrustLondon, UK
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24
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Soo Han J, Dug Lim S, Hyeok Choi W, Chul Hong S, Hee Park J, Park E, Jin Hong M, Lee CI, Hwan Park J, Ho Lee J, Oh Song J, Il Jo Y. Association of acute tubular necrosis with gross hematuria in cirrhosis-related immunoglobulin A nephropathy. Kidney Res Clin Pract 2013; 32:43-6. [PMID: 26889437 PMCID: PMC4716105 DOI: 10.1016/j.krcp.2012.12.003] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/14/2012] [Revised: 07/13/2012] [Accepted: 07/31/2012] [Indexed: 12/01/2022] Open
Abstract
Immunoglobulin A (IgA) nephropathy associated with cirrhosis is the most common form of secondary IgA nephropathy (IgAN). Cirrhosis-related IgAN is usually clinically silent with a rare occurrence of gross hematuria, unlike in cases of idiopathic IgAN. Especially, acute tubular necrosis (ATN) associated with gross hematuria is very rare in cirrhosis-related IgAN, although acute renal failure is a frequently reported complication in advanced cirrhosis. Herein, we report an unusual case of ATN requiring renal replacement therapy, associated with gross hematuria in a patient with nonalcoholic, hepatitis B virus-associated cirrhosis. Results of a histopathological analysis revealed obstruction of the lumen of renal tubules by red blood cell casts, a marked tubular necrosis, and IgA deposition in the mesangium. The patient's renal function and gross hematuria were clearly improved after lamivudine treatment.
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Affiliation(s)
- Jang Soo Han
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - So Dug Lim
- Department of Pathology, Konkuk University School of Medicine, Seoul, Korea
| | - Won Hyeok Choi
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Sung Chul Hong
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Jung Hee Park
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Eugene Park
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Mi Jin Hong
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Cho I Lee
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Jung Hwan Park
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Jong Ho Lee
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Jong Oh Song
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
| | - Young Il Jo
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
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25
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Lau C, Martin P, Bunnapradist S. Management of renal dysfunction in patients receiving a liver transplant. Clin Liver Dis 2011; 15:807-20. [PMID: 22032530 DOI: 10.1016/j.cld.2011.08.001] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Renal dysfunction is a frequent complication in patients with endstage liver disease awaiting orthotopic liver transplantation. Although the stereotypical form of renal dysfunction is the hepatorenal syndrome, common causes of acute kidney injury include prerenal azotemia and acute tubular necrosis in this population. Management involves hemodynamic support, renal replacement therapy, and mitigation of risk factors. Renal dysfunction in a cirrhotic patient usually implies a poor prognosis in the absence of liver transplantation. An important issue is the frequent need for kidney, in addition to liver, transplantation if renal insufficiency has been persistent in a decompensated cirrhotic.
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Affiliation(s)
- Christine Lau
- Kidney and Pancreas Transplant Program, Division of Nephrology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90024, USA
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26
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Nakayama M, Kaizu Y, Uesugi N, Nakashita S, Suehiro T. A case of IgA nephropathy and renal hemosiderosis associated with primary hemochromatosis. Ren Fail 2009; 30:813-7. [PMID: 18791957 DOI: 10.1080/08860220802249033] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/21/2022] Open
Abstract
IgA nephropathy associated with liver cirrhosis is a common disease, unlike hemochromatosis-associated renal involvement, which is uncommon. A 55-year-old man was admitted to our hospital for the acute deterioration of renal function. Laboratory tests showed extremely high transferrin saturation and serum ferritin level. Furthermore, magnetic resonance imaging revealed low-intensity signals in both T1- and T2-weighted images within the liver, diagnosed as primary hemochromatosis. Renal biopsy showed mesangial IgA deposition with cellular crescent and hemosiderin in both glomerular and tubular epithelial cells. Renal function worsened progressively after admission, and thus steroid pulse therapy was started. Renal dysfunction improved, but the patient died of cerebral hemorrhage. The present case was considered IgA nephropathy and renal hemosiderosis secondary to primary hemochromatosis. To our knowledge, this is the first report that describes the above complications in association with primary hemochromatosis.
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Affiliation(s)
- Masaru Nakayama
- Department of Internal Medicine, National Kyushu Medical Center Hospital, Division of Nephrology, Clinical Research Institute, Fukuoka, Japan
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27
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Koivuviita N, Tertti R, Heiro M, Metsärinne K. A case report: a patient with IgA nephropathy and coeliac disease. Complete clinical remission following gluten-free diet. NDT Plus 2009; 2:161-3. [PMID: 25949317 PMCID: PMC4421339 DOI: 10.1093/ndtplus/sfn205] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2008] [Accepted: 12/16/2008] [Indexed: 11/14/2022] Open
Affiliation(s)
- Niina Koivuviita
- Department of Medicine , Turku University Hospital , Turku , Finland
| | - Risto Tertti
- Department of Medicine , Turku University Hospital , Turku , Finland
| | - Maija Heiro
- Department of Medicine , Turku University Hospital , Turku , Finland
| | - Kaj Metsärinne
- Department of Medicine , Turku University Hospital , Turku , Finland
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28
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Abstract
IgA nephropathy (IgAN) is the most common pattern of primary glomerulonephritis seen in the Western world. In the majority of cases the cause remains unknown. Cases of familial IgAN and secondary IgAN have been reported and these have provided insights into underlying genetic and environmental triggers for this common glomerular disease. Secondary IgAN is seen most commonly in patients with liver disease or mucosal inflammation, in particular affecting the gastrointestinal tract. A number of dietary and microbial antigens have been identified in circulating IgA immune complexes and mesangial IgA deposits, suggesting that environmental factors may play a role in the pathogenesis of IgAN. There is an increasing literature reporting associations between IgAN and other diseases. Whether these reports represent chance associations or genuine shared pathophysiology is discussed.
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Affiliation(s)
- Shideh Pouria
- Renal Unit, New Guy's House, Guy's Hospital, London, United Kingdom
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29
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Almogren A, Kerr MA. Irreversible aggregation of the Fc fragment derived from polymeric but not monomeric serum IgA1—Implications in IgA-mediated disease. Mol Immunol 2008; 45:87-94. [PMID: 17606293 DOI: 10.1016/j.molimm.2007.05.002] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/20/2007] [Revised: 05/08/2007] [Accepted: 05/09/2007] [Indexed: 11/23/2022]
Abstract
IgA is by far the most abundant immunoglobulin in humans. It is found in serum and in secretions (SIgA). Unlike any other class of immunoglobulin, each form of IgA occurs naturally in different polymerisation states. In serum, the predominant form of IgA is IgA1 of which around 90% is monomeric and 10% is dimeric or polymeric. The proportion of dimeric/polymeric IgA increases in a number of important diseases, such as IgA nephropathy and in chronic liver disease. In both, there is evidence that further aggregation of dimeric/polymeric IgA is the cause of the characteristic tissue deposition. To investigate the effect of role of IgA polymerisation on the structure and function of IgA, we purified different molecular forms of IgA1 from myeloma serum (monomer, dimer and trimer) and SIgA1 from colostrum. Structural features of these different IgA1 forms were examined following proteolysis using Neisseria gonorrhoeae IgA1 type 2 protease and Streptococcus pneumoniae IgA1 protease. These IgA1 proteases cleave IgA1 at the hinge region and produce Fcalpha and Fab fragments. Western blot analysis demonstrated that the Fcalpha fragments of serum dimeric and trimeric but not monomeric IgA1 aggregated to form multimers resistant to disruption in SDS-PAGE under non-reducing conditions. Size exclusion chromatography under native conditions of cleaved serum dimeric IgA1 demonstrated that aggregation occurs because of structural changes in the IgA per se and was not an effect of the SDS-PAGE system. In the same assay, SIgA1 (dimeric) did not aggregate after digestion. The results suggest an important, previously unrecognised, property of dimeric/polymeric serum IgA1, which might explain its propensity to aggregate and deposit in tissues.
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Affiliation(s)
- Adel Almogren
- Department of Pathology, Immunology Unit, College of Medicine and King Khalid University Hospital, P.O. Box 2925, Riyadh 11461, Saudi Arabia
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30
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Kalambokis G, Christou L, Stefanou D, Arkoumani E, Tsianos EV. Association of liver cirrhosis related IgA nephropathy with portal hypertension. World J Gastroenterol 2007; 13:5783-6. [PMID: 17963311 PMCID: PMC4171271 DOI: 10.3748/wjg.v13.i43.5783] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
A high incidence of IgA nephropathy has been reported in patients with liver cirrhosis, though, clinically evident nephrotic syndrome is very uncommon. Impaired hepatic clearance of circulating IgA immune complexes and subsequent deposition in renal glomeruli has been considered principally in the pathogenesis of liver cirrhosis associated IgA nephropathy. Here we report on a patient with cryptogenic liver cirrhosis and splenic vein thrombosis, who presented with nephrotic syndrome. Renal biopsy showed findings consistent with IgA nephropathy. Lower endoscopy showed features of portal hypertensive colopathy. Following initiation of propranolol and anticoagulant treatment to reduce portal pressure, a gradual decrease of proteinuria and hematuria to normal range was noted. The potential pathogenetic role of portal hypertension in the development of IgA nephropathy in cirrhotic patients is discussed.
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31
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Luedde T, Trautwein C, Mehal WZ, Imaeda AB, Mehal WZ. Immunology of the Liver. TEXTBOOK OF HEPATOLOGY 2007:312-331. [DOI: 10.1002/9780470691861.ch2g] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
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32
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Szigeti N, Kovács T, Degrell P, Fábián G, Wittmann I, Nagy J. [Secondary IgA-nephropathy in gastroenterological diseases]. Orv Hetil 2007; 148:313-8. [PMID: 17344151 DOI: 10.1556/oh.2007.27984] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/19/2022]
Abstract
IgA-nephropathy is the most common primary chronic glomerulonephritis worldwide. Beside the primary IgA-nephropathy (IgA-nephropathy with an unknown origin), there are more and more cases, which are associated with diseases of other organs. Although the causality is often not obvious, these forms are called secondary IgA-nephropathy. In this study, the authors cover only the secondary forms of IgA-nephropathy with relation to gastroenterology in a broader sense that includes the liver. They would like to draw the attention to the necessity of analyzing also the associate occurrence of gastrointestinal diseases (principally liver diseases, coeliac disease, Crohn's disease, ulcerative colitis) in patients with IgA-nephropathy, as well. They think that it would be expedient to organize a nationwide clinical analysis that would search the frequency of occurrence of IgA-nephropathy in the above mentioned gastrointestinal diseases.
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Affiliation(s)
- Nóra Szigeti
- Pécsi Tudományegyetem, Altalános Orvostudományi Kar, II. Belgyógyászati Klinika és Nefrológiai Centrum, Pécs.
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