Diabetic Nephropathy, or not?

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A man in his 30s with a history of type 1 DM and chronic
hypokalemia 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 proteinuria
or hematuria.  His renal biopsy showed
focal tubular atrophy, dystrophic calcification in the scattered tubules, and
did not have any signs of diabetic nephropathy.  His renal biopsy findings were therefore attributed to
chronic hypokalemia.
Hypokalemia can cause kidney damage if it persists for longer
than one month.   Chronic hypokalemia can
cause non-specific vacuolar lesions in the epithelial vessels in the proximal
tubules.  Typical renal biopsy will show
interstitial nephritis, fibrosis, tubular atrophy and cyst formation.  The pathogenesis of hypokalemic nephropathy
is not clear.  The hypotheses are:  1) complement activation and tubular cell
damage by hypokalemia induced renal ammonium production 2) stimulation of cell growth and proliferation by intracellular acidosis 3) increased production of growth
factors (VEGF, IGF-1) and cytokines by hypokalemia through an uncertain mechanism.
After further work-up, our patient was diagnosed with Giltelman
syndrome.  He was
started on potassium replacement and his Cr has remained stable since then.  
Posted by Jie Cui


  1. His serum potassium was round 2.6-2.8 mg/dl before referred to renal. His serum magnesium level was normal. He did not have any history of nausea or vomiting. No suspicious for inappropriate diuretic use. We send 24 hour urine lytes, which showed low urine calcium. Gitelman is the most likely diagnosis.
    Actually, his renal function has been stable in the past 10 years.



  2. I'll try to get those details and pass them on to you.

  3. Interesting. What was his magnesium level? How was the diagnosis of Gitelmans syndrome entertained? thanks

  4. Very interesting. What was his potassium level? I looked but did not see it mentioned.

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