Possible Role for Impaired Renal Prostaglandin Production in Pathogenesis of Hyporeninæmic Hypoaldosteronism

Norby, L H; Ramwell, Peter W.; Weidig, J.; Slotkoff, Lawrence M.; Flamenbaum, Walter

doi:10.1016/s0140-6736(78)92275-4

Cited by 40 publications

(7 citation statements)

References 20 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: 93%

“…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. In our patients with hypoaldosteron ism, 7 had urinary PGE2 excretion rates that were lower than the values determined in the two control groups.…”

Section: Discussionmentioning

confidence: 99%

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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: 93%

Section: Discussionmentioning

confidence: 99%

Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Kaufman¹,

Peck²,

Hamburger³

et al. 1986

Nephron

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“…39 suggested that a switch in intrarenal synthesis of prostaglandins from prostaglandin Ej to F 2 could explain the features of Gordon's syndrome. Fichman et al 40 had proposed an etiological role for prostaglandin excess in Banter's syndrome, as had Norby et al 41 for prostaglandin deficiency in their patient with hyporeninemic hypoaldosteronism. Sanjad et al 8 reported very low urinary excretion of prostaglandin Ej in their patient with Gordon's syndrome, which was increased 20-fold by treatment with orally administered furosemide.…”

Section: Uringj 4 7 12 13 15 16 18 19 21 ^J T Q E X C R E T mentioning

confidence: 97%

Syndrome of hypertension and hyperkalemia with normal glomerular filtration rate.

Gordon¹

1986

Hypertension

206

121

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“…Both the hyperkalemia and low renin and aldosterone levels were reversible following indomethacin withdrawal. Two subsequent studies re ported diminished urinary prostaglandin E levels in patients with hyporeni nemic hypoaldosteronism (135,136), but this observation has been challenged by others (137,138). Further studies will be needed to clarify these apparently conflicting reports.…”

Section: Impaired Renin-aldosterone Axismentioning

confidence: 99%

Clinical Disorders of Hyperkalemia

DeFronzo¹,

BIa²,

Smith³

1982

Annu. Rev. Med.

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Potassium DistributionTotal body potassium in a healthy adult is approximately 50 meqlkg body weight or about 3500 meq for a 70-kg man (1, 2). Most of this is located within cells (Figure 1), primarily muscle, at a concentration of about 150 meq/L. Only 2% of total body potassium is located in the extracellular fl uid, normally at concentrations of 3.5 -5.0 meq/L. The maintenance of this high intracellular to extracellular K concentration depends upon the Na-K ATPase pump (3, 4) as well as other fac tors, including H+ balance, plasma tonicity, and plasma insulin, epinephrine, and aldosterone concentrations (5). The large difference in potassium concentration across the cell mem brane is critical for normal cell fu nction since it is the primary determinant of the resting membrane potential. Small changes in the intracellular/ex tracellular K ratio can severely disturb neuromuscular fu nction, particu larly of the heart. A gain (or loss) fr om the extracellular space of an amount of potassium equal to only I % of the total body K content (35 meq) can cause a 50% increase (or decrease) in plasma K concentration. Such a change would have pronounced effects on neuromuscular func ti on. Like wise, redistribution of a similar amount of potassium fr om the intracellular to extracellular (or vice versa) fluid compartmen t without net gain or loss of K fr om the body, would similarly affect neuromuscular excitability. Thus, it is important that both the total amount of potassium within the body and the distribution of potassium between intracellular and extracellu lar fl uid compartments be closely regulated.In healthy man, potassium enters only via the gastrointestinal tract. Approximately 100 meq of K is ingested per day and essentially all of this is absorbed fr om the stomach and upper gastrointestinal tract. Approxi-521 0066-4219/8 2/040 1-0521 $02.00 Annu. Rev. Med. 1982.33:521-554. Downloaded from www.annualreviews.org Access provided by Haifa University on 01/05/15. For personal use only.Quick links to online content Further ANNUAL REVIEWS

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Possible Role for Impaired Renal Prostaglandin Production in Pathogenesis of Hyporeninæmic Hypoaldosteronism

Cited by 40 publications

References 20 publications

Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Syndrome of hypertension and hyperkalemia with normal glomerular filtration rate.

Clinical Disorders of Hyperkalemia

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