HDCN Abstract:  Am Soc Nephrol Ann Mtg -- Toronto  

Chan C, Lin SH, Halperin ML

Why lesions of the loop of Henle (LOH) cause renal potassium (K) wasting

Am Soc Nephrol Ann Mtg -- Toronto
J Am Soc Nephrol (Sep) 11:103A 2000

Background: While the cortical collecting duct (CCD) controls K excretion, patients with Bartter's syndrome (BS) have a defect in NaCl reabsorption in the LOH, but they have hypokalemia due to renal K wasting with a high urine [K].

Objective: To evaluate when furosemide (F) can mimic the pattern of augmented renal excretion of K that is seen in patients with BS.

Methods: Normal humans (n=16) were given DDAVP and sufficient F to cause a >500 % increase in Na excretion. 6 patients with congestive heart failure (CHF) and hypokalemia (K=3.1±0.2 mM) received F. K excretion and the transtubular [K] ratio (TTKG) were measured.

Rats (n= 30) were placed on a low K diet. They were given 15 mg F/kg q8h for 3-4 days. Urines were collected q8h. Na citrate was added to the drinking water instead of NaCl on days 2 + 3 to study the role of metabolic alkalosis (MAlk) on K excretion because patients with BS have MAlk.

Results: Normal humans given F had a urine [Na] and [K] of 147±5 & 7±1 mM, respectively (TTKG < 2).

Patients with CHF had a urine [Na] of 71±8.8 mM and a plasma [K] of 31 ± 4.6 mM, and a TTKG of 11±1.7 after F.

In rats, the 1st dose of F caused the urine [K] to be 6±1 mM. When a negative Na balance was present in rats, the urine [K] was in the mid 50 mM range with TTKG >10. When MAlk was induced, there was a fall in the plasma [K], a fall in the K excretion rate, and a marked fall in the TTKG to 2.0.

Conclusions: Renal K wasting, a high TTKG, and hypokalemia occur with a LOH lesion only if there is also an increased avidity of Na reabsorption in the CCD as in BS.
Metabolic alkalosis diminishes renal K wasting only if the plasma [K] falls to the mid 2 mM range. This helps minimize the actual K deficit.

Copyright 2000, American Society of Nephrology