Human kidney histopathology in acute obstructive jaundice

Abstract

This study is the first in the literature to address the histopathological changes that occur in humans with short-term biliary obstruction. Acute tubular necrosis and venous dilatation was observed in all biopsies, without exception, despite the maintenance of strict volume control in all patients. The adequacy of volume control may not be implicated in those results; rather a possible mechanism related to untrapped endotoxin in the gut lumen or systemic circulation might lead to prolonged PTC dilatation and hypoperfusion with synchronous acute tubular necrosis. Absolute recovery of renal function in all patients and the demonstration of solitary acute tubular necrosis with no microvascular-glomerular-interstitial inflammation or injury, suggests that the perioperative treatment regime in this study is fairly efficacious in short-term OJ.

Bile Acid-Induced Cholemic Nephropathy

“…fulminant AIH). Interestingly, and in contrast to the study by Uslu et al [73], the presence of bile casts in these patients significantly correlated with the degree of jaundice (total and direct bilirubin levels). It is important to note that 13 of 44 patients in the study were clinically classified as having HRS; however, 11 (85%) out of these 13 patients showed bile casts upon kidney histology.…”

“…As such, Uslu et al [73] published a prospective study in 20 patients with short-term obstructive jaundice (mean duration of biliary obstruction of 15 days, mean total bilirubin: 10.1 ± 1.0 mg/dl), and demonstrated that those patients frequently showed acute tubular necrosis and venous dilatation upon renal biopsies despite maintenance of strict perioperative volume control and normal to only slightly impaired renal function (preoperative serum creatinine: 0.97 ± 0.1 mg/dl, mean GFR determined by MDRD equation: 81.9 ± 0.4 ml/min). Their study did not show a correlation between severity of jaundice (total bilirubin levels) and severity of the tubular and vascular changes observed.…”

“…Besides intraluminal bile casts and tubular injury, the presence of mononuclear inflammatory cells in the vasa recta has been reported [33]. Data on glomerular alterations in obstructive jaundice and CN are scarce and limited to only a few reports on mesangial C3, glomerular C4d and IgA deposition, and hyperplasia of the parietal layer of Bowman's capsule [45,73,74]. Key histomorphological characteristics of CN are shown by the example of hematoxylin and eosin-, PAS- and Sirius red-stained kidney sections of an 8-week common bile duct-ligated mouse in figure 1.…”

The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine

“…Several studies have shown that multiple organ injury occurs in CC [6–8]. CC with liver dysfunction is frequently accompanied by kidney injury [9–12], which could be caused by endotoxemia, vasoactive mediators, and free radicals [13–15]. In addition, renal injury associated with liver diseases could occur by direct tubular toxicity or nephron obstruction [16].…”

Efficacy of extracorporeal albumin dialysis for acute kidney injury due to cholestatic jaundice nephrotoxicity

“…Acute kidney injuries (AKI) in patients with severe jaundice have often been reported 1 2. This has led the medical community to consider cholestasis as a cause of renal failure, and to classify this mechanism of injury under the term, ‘cholemic nephropathy’.…”