A man in his 30s with a history of type 1 DM and chronichypokalemia was referred to the renal clinic for investigation of CKD. His creatinine was 1.8g mg/dl. His DM was well controlled without any evidence of retinopathy. Urinalysis did not show any proteinuriaor hematuria. His renal biopsy showedfocal tubular atrophy, dystrophic calcification in the scattered tubules, anddid not have any signs of diabetic nephropathy. His renal biopsy findings were therefore attributed tochronic hypokalemia. Hypokalemia can cause kidney damage if it persists for longerthan one month. Chronic hypokalemia cancause non-specific vacuolar lesions in the epithelial vessels in the proximaltubules. Typical renal biopsy will showinterstitial nephritis, fibrosis, tubular atrophy and cyst formation. The pathogenesis of hypokalemic nephropathyis not clear. The hypotheses are: 1) complement activation and tubular celldamage by hypokalemia induced renal ammonium production 2) stimulation of cell growth and proliferation by intracellular acidosis 3) increased production of growthfactors (VEGF, IGF-1) and cytokines by hypokalemia through an uncertain mechanism.
After further work-up, our patient was diagnosed with Giltelmansyndrome. He wasstarted on potassium replacement and his Cr has remained stable since then.
Posted by Jie Cui
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