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Cebeci E, Ekinci I, Gursu M, Coskun C, Karadag S, Uzun S, Behlul A, Senel TE, Kazancioglu R, Ozturk S: Podocyte Injury in Autosomal Dominant Polycystic Kidney Disease. Nephron DOI: 10.1159.000499741

Autosomal dominant polycystic kidney diseases (ADPKD) is generally regarded as a prototypical hereditary tubulo-interstitial kidney disease.

Glomerular alterations have received little attention.

Cebeci and colleagues help to fill this gap in information by conducting an observational (non-biopsy) study of urinary biomarkers of podocyte injury, specifically podocin (P) and podocalyxin (PC), in patients with ADPKD and healthy controls. They found increased excretion of P and PC (measured as urine concentration indexed to creatinine in ng/mg) in ADPKD compared to controls, especially in the presence of decreased eGFR or proteinuria. As expected about 2/3rds of the ADPKD were hypertensive. The P and PC levels correlated with urine protein creatinine ratio (UPCR) but not with hypertension or its treatment.

These findings suggest ongoing glomerular (podocyte) injury in ADPKD, but do not answer question about this injurious process to the rate of decline in eGFR in ADPKD. The pathological process in ADPKD include slow decline in the nephron population and compensatory hypertrophy in residual, spared nephrons. This compensation may exact consequences, like mechanical-stress induced podocyte injury. Thus, in a sense, these findings were predictable. Whether monitoring of podocyte injury by urinary P or PC will be useful as a prognostic tool, like total kidney volume by MRI, in ADPKD cannot be answered by a study of this design. Longitudinal studies would be required, but such an analysis might be reasonable going forward.

Quoted Karger Article

Podocyte Injury in Autosomal Dominant Polycystic Kidney Disease

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