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Prolonged cholestasis, characterized by retention of bile compound, may cause renal damage, which sometimes leads to renal failure.
However, experimental data show that hyperchloraemia may cause renal vasoconstriction in a manner proportional to severity [76 78].
The pathophysiology of rhabdomyolysis-induced AKI is believed to be triggered predominantly by myoglobin, which may cause renal dysfunction by direct renal cytotoxicity after reaching the tubules [4], vasoconstriction and tubular obstruction [1, 5].
In immunocompromised hosts reactivation of the JCV infection is the cause of the central nervous system disease progressive multifocal leucoencephalopathy (PML), while BKV may cause renal nephropathy and haemorrhagic cystitis.
NSAIDs may cause renal failure or renal issues.
Each component of metabolic syndrome, per se, may cause renal function damage [ 10].
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It may still cause renal scar formation in up to 40% of cases, leading to hypertension, proteinuria, and end-stage renal disease in children [ 3].
High F− doses may also cause renal toxicity (Zager and Iwata 1997), epithelial lung cell toxicity (Thrane et al. 2001), and reproductive defects (Ghosh et al. 2002).
Although HCV co-infection may also cause renal injury, the undetectable HCV viral load and positive Leishmania infantum PCR suggested that MPGN was more likely to be linked to VL than to HCV.
Myoglobin is a heme containing compound with a molecular weight of 17,400 Daltons and may cause acute renal failure by tubular obstruction, toxicity of heme pigments, renal ischemia and decreased glomerular permeability [2].
CCE, induced by cholesterol crystals dispersed from atherosclerotic plaques of the aorta [2], may cause chronic renal failure, blue toe, livedo reticularis, and intestinal ischemia with perforation, stenosis, or inflammatory mass formation [1, 6, 7].
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