Metabolic observations on salt wasting in a patient with renal disease

Obstructive sodium-losing nephropathy--a case report and review

“…In other cases (Morgan et al, 1978) loss of skin elasticity was not described. However, both these patients and the present one showed signs of diminished plasma volume but not pigmentation as reported by others (Walker et al, 1965). Nephrocalcinosis and hypertension were considered possible causes of her sodium depletion but plasma and urinary calcium were normal, no calcification was seen on abdominal X-ray, regular anti-hypertensive treatment had been prescribed during out-patient follow-up, she was not hypertensive on admission and had no signs of hypertensive disease; in particular, chest radiology and fundoscopy were normal although electrocardiography suggested left ventricular strain.…”

Granulomatous Interstitial Nephritis and Uveitis Presenting as Salt-Losing Nephropathy

“…With tubular destruction nephrons with long loops of Henle and greater sodium reabsorptive capabili ties are lost resulting in salt wasting. Finally, an unidenti fied natriuretic hormone may be involved in the intracta ble salt wasting [14], We presume this patient's salt was tage was due to tubulointerstitial disease.…”

Salt-Losing Nephropathy

“…2 patients in this review [5,38] presented with serum K of 2.0 and 3.1 mEq/1. Both patients had severe meta bolic acidosis and their minimum urinary pH levels were 5.5 and 6.0, findings suggestive of renal tubular acidosis.…”

“…In 5 patients [11,14,21,36,37] serum K was between 4 and 5 mEq/1 but it rose to 6, 7 and 8 mEq/1 in 3 of them within a few days. 2 patients [5,38] presented with significant hypokalemia, with serum K levels of 2.0 and 3.1 mEq/1, respectively. 1 of the 15 patients [13] whose serum K was never mea sured, had persistent EKG changes characteristic of hy perkalemia.…”

“…Patients with chronic renal failure commonly have decreased ability to conserve salt [1,2], However, in a very small number of them this impairment is so severe and prominent that their clinical state has been called salt-losing or salt-wasting nephropathy [3], The mecha nisms proposed for excessive salt loss include ureainduced osmotic diuresis [4], glomerulotubular imbal ance [5], and impairment in tubular salt reabsorption [6,7], The first is not tenable since osmotic diuresis is present in all patients with renal failure and also since the salt loss is far in excess of that achievable by urea excre tion. Glomerulotubular imbalance denotes excessive glo merular filtration rate per remaining nephron without comparable increase in tubular salt reabsorption.…”