Indomethacin-Induced Hyperkalemia and Renal Failure in Multiple Myeloma

Paladini, G; Tonazzi, C.

doi:10.1159/000206989

Cited by 11 publications

(3 citation statements)

References 13 publications

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“…Several theories have been suggested, includ ing damage to the juxtaglomerular apparatus [1,2,7], impaired sympathetic nervous system stimulation [1,2,24], suppression by volume expansion [1,2,6], impaired conversion of 'prorenin' to renin [1,2,[8][9][10], and altera tions in prostaglandin synthesis [1,2,9,11,14,15]. We examined the last two mechanisms in the present study.…”

Section: Discussionmentioning

confidence: 94%

“…PGE2 may stimulate renin release in vivo and in vitro [31] and may have a role in modulating aldoste rone secretion independent of its effects on renin release [32]. Numerous case reports have documented the occur rence of the syndrome of isolated hypoaldosteronism in patients ingesting nonsteroidal anti-inflammatory drugs, known inhibitors of prostaglandin synthesis [14,15]. In addition, Norbyet al [11] have reported a patient with the syndrome who had a low urinary prostaglandin excretion and who increased her plasma aldosterone and de creased her plasma potassium concentration during an infusion of PGA.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, several cases of hyperkalemic, hyper chloremic metabolic acidosis typical of isolated hypoaldosteronism have been reported after the admin istration of nonsteroidal anti-inflammatory drugs, known inhibitors of prostaglandin synthesis [5,14,15]. In the present study, we measured urinary kallikrein and prostaglandin E2 (PGE2) excretion and plasma inactive renin in patients with isolated hypoaldosteronism to fur ther elucidate the pathophysiology of this syndrome.…”

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confidence: 91%

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Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Kaufman¹,

Peck²,

Hamburger³

et al. 1986

Nephron

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To further define the pathophysiology of the syndrome of acquired isolated hypoaldosteronism, we determined plasma concentrations of active and inactive renin and urinary kallikrein and prostaglandin E₂ excretion rates in 11 patients with the syndrome, 12 patients with similar serum creatinine levels, but without hyperkalemia, and in 12 normotensive patients with normal renal function and low plasma renin activities (PRA). Ten of 11 patients with the syndrome had low baseline PRA, and, unlike the control groups, six of 11 failed to double their PRA after furosemide stimulation. There were also consistent abnormalities in the percentage of inactive renin, no patient having a value less than and no control subjects having a value greater than 65%. Seven of 11 patients had prostaglandin E₂ excretion rates lower than either control groups. Urinary kallikrein excretion rates in the patients with isolated hypoaldosteronism were significantly lower than in the control groups, but increased in response to therapy with fludrocortisone.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 91%

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Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Kaufman¹,

Peck²,

Hamburger³

et al. 1986

Nephron

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Nonsteroidal Anti‐Inflammatory Drugs: Effects on Kidney Function

Whelton

Hamilton²

1991

The Journal of Clinical Pharma

295

123

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are capable of inducing a variety of renal function abnormalities, particularly in high-risk patients with decreased renal blood perfusion who depend on prostaglandin synthesis to maintain normal renal function. Fluid retention is the most common NSAID-related renal complication, occurring to some degree in virtually all exposed individuals; however, clinically detectable edema occurs in less than 5% of patients and is readily reversible on discontinuation of the NSAID. Other electrolyte complications, notably hyperkalemia, are seen infrequently and occur in specific at-risk patients. The next most worrisome complication is acute deterioration of renal function, which occurs in high-risk patients and is also reversible. Nephrotic syndrome with interstitial nephritis is a rare problem of NSAID use and is reversible. Papillary necrosis is the only permanent complication of NSAIDs and is very rare. Altogether, these renal function abnormalities, with the exception of mild fluid retention, are clinically detectable in approximately 1% of exposed patients. Given the number of patients who take NSAIDs on a prescription or over-the-counter basis, the absolute number of at-risk patients is relatively large. Consequently, an appreciation for the risk factors and pathophysiology of NSAID-induced renal function abnormalities is required for optimal use of these drugs.

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