An electronmicroscopic study of experimental hematogenous pyelonephritis

Petorak, I.; Iplikci, Altan; Öbek, A.; Anǧ, Özdem; Büget, Ergene

doi:10.1016/s0014-4908(76)80041-5

Cited by 3 publications

(1 citation statement)

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“…Obgleich die Tubulusatrophie eine bekannte und haufig untersuchte Lasion des Nierengewebes darstellt, sind bislang nur Teilaspekte und einzelne Schritte der formalen Pathogenese beschrieben worden. So wurden in den letzten Jahren Phanomene der Entdifferenzierung [5, 291, die Bedeutung der tubularen Basalmembran [ 18, 221 und die Rolle der Lysosomen am Epitheluntergang [ 17,20,231 hervorgehoben.…”

Section: Demonstratedunclassified

Die Kaliumhydrogenphosphat-induzierte Nephropathie des Hundes. I. Pathogenese der Tubulusatrophiee [Potassium Hydrogen Phosphate Induced Nephropathy in the Dog. I. Pathogenesis of Tubular Atrophy—author's trans.]

et al. 1980

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Abstract. A nephropathy with severe tubular atrophy was observed in Beagle dogs after oral administration of K2HP04 for 14 or 38 weeks. We describe the complete lysosomal degradation of atrophying tubular epithelial cells.During two experiments of 14 and 38 weeks duration, respectively, a total of 15 Beagle dogs received 0.8 g KnHPOJkg body weight daily with their food. All dogs were examined clinically at regular intervals. Renal biopsies were taken in the fourth week from beagles of the 14-week study. Results were compared with those of control dogs. At the end of the experiments the animals were killed and necropsies done. Different stains and histochemical reactions were applied to paraffin sections of the kidneys. Acid phosphatase and P-glucuronidase were found on cryostat sections. Kidneys futed by perfusion of five Beagles from the 38-week study and three Beagles of the 14-week study, and from five control dogs, were examined electron microscopically. Ultrahistochemically, acid phosphatase was demonstrated.Clinically, the dogs in both experiments vomited, were cachectic, and had elevated creatinine and blood urea nitrogen. Morphologically, qualitatively identical changes were seen, but the renal damage was most marked at 38 weeks. There were disseminated tubular atrophy (usually of the proximal tubules), focal scar tissue and nephrocalcinosis. The following pathogenesis was established for the lesions of the proximal tubule: Tubular atrophy begins with loss of differentiation of epithelial cells. Enzyme histochemistry, ultrahistochemistry and electron microscopy show an increase in autophagic vacuoles and autophagolysosomes. The lysosomal bodies showing fusion enclose large parts of the cytoplasm as the process continues. Complete lysosomal degradation of epithelial cells and extrusion of large lysosonies into the tubular lumen follow. After complete enzymatic digestion of the intratubular detritus, the residue is empty, convoluted and collapsed tubular basement membrane. Atrophic tubular epithelial cells have many organelle-free zones at their base, which contain fine filamentous material resembling that of the basement membrane.The degradation processes described here may explain why clinically the urinary sediment contains few cylinders and epithelial cells and why proteinuria decreases significantly toward 699

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Section: Demonstratedunclassified