Chronic renal insufficiency and Nocardia brasiliensis infection: A call for heightened vigilance and multidisciplinary management

Table 1 The complex interplay among chronic kidney disease, hypertension, and gout significantly impacts immune function through various mechanisms

Factor	Mechanism of action	Specific manifestations	Impact on immune function
CKD	Reduced renal function leads to accumulation of uremic toxins	Uremic toxins directly impair macrophage activity	Weaken the body’s first line of defense against pathogens, reduce macrophage phagocytic capacity
Hypertension	No direct mechanism specified, but often coexists with CKD and gout	Commonly managed with immunosuppressive agents (e.g., corticosteroids)	Exacerbate neutrophil dysfunction, impact early immune response
Gout	Hyperuricemia triggers inflammatory responses	Urate crystal deposition induces local inflammation and activates the immune system	Promotes inflammation and immune dysregulation, may further affect immune cell function
Immunosuppressive agents	Commonly used in the management of these comorbidities	Suppress immune cell functions, particularly neutrophils	Exacerbate neutrophil dysfunction, reduce the body’s ability to fight infections

CKD: Chronic kidney disease.

Table 2 Diagnostic and therapeutic innovations in Nocardia brasiliensis infection

Aspect	Key innovations	Impact
Diagnostic modalities	MALDI-TOF MS: Rapid species identification (< 1 hour)	Reduced time-to-treatment compared to culture-based methods
	mNGS: Detection of polymicrobial infections and co-pathogens (e.g.,Pneumocystis jirovecii)	Enhanced diagnostic yield in immunocompromised hosts
	E-test: Guided antibiotic susceptibility testing	Optimized SMZ-TMP dosing based on local resistance patterns
Therapeutic strategies	Low-dose SMZ-TMP: Reduced nephrotoxicity risk in CRI patients	Improved tolerability and adherence in elderly populations
	Surgical drainage: Adjunctive management of cutaneous abscesses	Hastened resolution of localized infections
	Pharmacokinetic monitoring: Targeted SMZ trough levels (50-100 μg/mL)	Minimized toxicity while

MALDI-TOF MS: Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry; mNGS: Metagenomic next-generation sequencing; SMZ-TMP: Sulfamethoxazole-trimethoprim; CRI: Chronic renal insufficiency; SMZ: Sulfamethoxazole.