Human kidney histopathology in acute obstructive jaundice: a prospective study.

INTRODUCTION

Cholemia and bacterial translocation with portal endotoxemia are integral in the pathogenesis of obstructive jaundice (OJ). There is sufficient experimental data about hemodynamic and histopathological consequences of OJ. In contrast, pathological information of renal changes in patients with OJ is still lacking. Therefore; the primary objective of this prospective study is to show the specific histopathological changes in kidneys of patients with short-term biliary tract obstruction receiving a standard perioperative medical treatment protocol.

MATERIALS AND

METHODS

Twenty consecutive patients with biliary obstruction were included in the study. Fluid replacement, prevention of biliary sepsis, and portal endotoxemia were mainstays of the perioperative treatment protocol. Fluid and electrolyte balance was maintained by twice daily body weight calculations, central venous pressure, and mean arterial pressure monitoring. Renal function was assessed by glomerular filtration rate estimation by modification of diet in renal disease-7 formula. Kidney biopsy evaluation was focused on tubular changes, thrombotic microangiopathy, endothelial damage, and peritubular capillary (PTC) dilatation with or without C4d staining. Fresh frozen sections were evaluated with immunofluorescence microscopy for glomerular IgG, IgA, IgM, C3, and C1q staining.

RESULTS

The mean duration of OJ was 15.5 ± 1.4 days. Body weight increased before surgery through volume expansion (P = 0.001). All patients have shown mean arterial pressure ≥ 70 and ≤ 120 mmHg and renal function was very well preserved in all but one subject during the perioperative period. Despite those favorable figures, dilatation of peritubular venules and acute tubular necrosis were shown synchronously in all cases. C4d staining in PTC and arterioles and thrombotic microangiopathy were entirely absent in the study group. Immune complex deposits in PTCs and in glomeruli were not detected. Three patients had isolated glomerular C4d deposition without accompanying thrombotic microangiopathy and IgG, IgA, IgM, C3, and C1q staining of glomerular capillaries in I immunofluorescence microscopy.

DISCUSSION: 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.