BACKGROUND: Hypokalaemic nephropathy has been described in patients with chronic 
potassium depletion; it is a condition in which proximal tubular vacuolization 
and interstitial fibrosis occur, resulting in a decline in glomerular filtration 
rate (GFR) and, in some cases, renal failure. It has been described in patients 
with chronic diarrhoea, eating disorders, laxative abuse and primary 
hyperaldosteronism; also occasionally in Bartter syndrome (BS), in which severe 
hypokalaemia accompanies significant renal sodium and water losses, though 
rarely in Gitelman syndrome (GS), in which there is equally severe hypokalaemia, 
but only modest sodium losses.
AIM: We hypothesized that hypokalaemic nephropathy may not be due to potassium 
depletion per se, but persistently elevated circulating levels of aldosterone, 
possibly with superimposed episodes of renal hypoperfusion.
DESIGN AND METHODS: We searched UK and European data sets to retrospectively 
compare serum and urinary parameters in patients with GS and BS.
RESULTS: The patients with GS often had lower serum potassium concentrations 
than patients with BS, but the BS patients had significantly higher serum 
creatinine concentrations and lower estimated GFRs (eGFR). BS patients had 
significantly higher fractional excretions of sodium compared with GS patients, 
as well as higher plasma renin activities and serum aldosterone levels.
CONCLUSION: These findings show that in genetically confirmed cases of BS and 
GS, the degree of hypokalaemia (as an index of chronic potassium depletion) does 
not correlate with GFR, and that on-going sodium and water losses, and 
consequent secondary hyperaldosteronism, may play a more important role in the 
aetiology of hypokalaemic nephropathy.