Chan C, Lin SH, Halperin ML
Why lesions of the loop of Henle (LOH) cause renal potassium
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
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
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
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.
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