Salt-Losing Nephropathy

Uribarri, Jaime; Oh, Man S.; Carroll, Hugh J.

doi:10.1159/000166709

Cited by 29 publications

(3 citation statements)

References 16 publications

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“…Kleeman et al [12] demonstrated that patients with chronic renal tubular damage seem to have a greater pro pensity for salt wasting than those with glomerular dis ease. In fact, salt-wasting nephropathy is more common in tubulointerstitial diseases like chronic pyelonephritis, renal tuberculosis, renal candidiasis and medullary cystic disease [4], The mechanism causing salt wastage is un clear but one suggestion is urea-induced osmotic diuresis in the setting of renal dysfunction [5,12], but patients with comparable degrees of renal dysfunction and azo temia do not demonstrate salt wasting. Moreover, this patient was excreting 3.5 g urea nitrogen per day with a (BUN) of only 36 mg/dl.…”

Section: Discussionmentioning

confidence: 99%

Granulomatous Interstitial Nephritis and Uveitis Presenting as Salt-Losing Nephropathy

et al. 1997

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Salt-wasting nephropathy is a rare syndrome in which renal insufficiency is associated with extracellular volume depletion from marked natriuresis in the absence of adrenal insufficiency or diuretics. We report the clinical course of a 23-year-old woman with renal insufficiency, in association with orthostatic hypotension and salt wasting. A combination of daily infusion of saline, a high-salt diet and oral fludrocortisone did not compensate for her salt loses. Renal biopsy showed noncaseating granulomas and marked interstitial inflammation. Renal function and salt loss improved with prednisone therapy and 6 months after withdrawal of steroids, her renal function remains stable.

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Section: Discussionmentioning

confidence: 99%

Granulomatous Interstitial Nephritis and Uveitis Presenting as Salt-Losing Nephropathy

et al. 1997

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“…The site of defective sodium transport does not appear to be the cortical collecting duct either, since such a defect should produce hyperkalemia as is the case in salt losing nephropathy [24]or pseudohypoaldosteronism [25]. Furthermore, plasma aldosterone levels should be markedly increased if the defect were at the cortical collecting duct.…”

Section: Site Of Salt Transport Defectmentioning

confidence: 99%

Cerebral Salt-Wasting Syndrome

Carroll²

1999

Nephron

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It is widely believed that the cerebral salt-wasting syndrome (CSWS) exists as an entity distinct from the syndrome of inappropriate ADH secretion, and that it is characterized by evidence of severe renal salt wasting that results in volume depletion and hyponatremia. Proof of the existence of CSWS as an entity requires documentation of renal salt wasting and volume depletion. The present review has been undertaken to examine the evidence that the CSWS is a separate entity. In this effort, we have discussed various methods of documentation of volume depletion, and then reviewed reported cases of CSWS to determine whether volume depletion and renal salt wasting have been clearly demonstrated. Our review has led us to conclude that not one case of purported CSWS has demonstrated clear evidence of volume depletion and renal salt wasting. If renal salt wasting had been proven in these cases, we would conclude that the likely site of renal salt transport was the proximal tubule. The proximal site of salt transport defect has been suggested by the absence of hyperreninemia and hypokalemia, which would be a distinguishing feature of Bartter’s syndrome and Gitelman’s syndrome.

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“…In this setting, electrolyte-free water is retained in the body, and extracellular fluid volume (ECV) is expanded. On the other hand, salt-losing nephropathy (SLN) is defined as a renal loss of sodium that leads to hyponatremia and ECV loss [2]. Differentiation of SLN from SIADH is important because treatment of SLN is opposite from that of SIADH.…”

Section: Introductionmentioning

confidence: 99%

Development of Severe Hyponatremia due to Salt-Losing Nephropathy after Esophagectomy for Esophageal Cancer

Yoshioka

Nishio

Sano

et al. 2009

Case Reports in Medicine

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A 72-year-old woman was admitted to our hospital for esophagectomy for esophageal cancer. On the third postoperative day, she developed polyuria (3.8 L/day), massive natriuresis, hyponatremia (112 mEq/L), hyperkalemia (5.6 mEq/L), and decreased central venous pressure, which was refractory to isotonic saline infusion. Laboratory findings indicated proximal tubular injury (high urinary β2-microglobulin, coexistence of hypouricemia) together with reduced aldosterone action at the cortical collecting duct. A diagnosis of salt-losing nephropathy was made and sodium correction was done with 3% saline and fludrocortisone. She responded well to therapy. The cause of hyponatremia was considered renal tubular dysfunction together with elevated antidiuretic hormone level. Postoperatively, it is important to look for the development of salt-losing nephropathy.

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Salt-Losing Nephropathy

Cited by 29 publications

References 16 publications

Granulomatous Interstitial Nephritis and Uveitis Presenting as Salt-Losing Nephropathy

Granulomatous Interstitial Nephritis and Uveitis Presenting as Salt-Losing Nephropathy

Cerebral Salt-Wasting Syndrome

Development of Severe Hyponatremia due to Salt-Losing Nephropathy after Esophagectomy for Esophageal Cancer

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