The effect of potassium loading on sodium excretion and plasma renin activity in Addisonian man.

Miller, Paul D.; Waterhouse, Catheryne; Owens, Robyn; Cohen, Edwin L.

doi:10.1172/jci108099

Cited by 19 publications

(5 citation statements)

References 35 publications

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“…The fact that a supplement of 100 mmol of potassium chloride did not significantly increase the PRA of our control subjects suggests that the response may depend upon the precise amount of potassium given. Studies of Addisonian patients found that the administration of 200 mmol of potassium chloride did not depress PRA, and suggested therefore that a fall in PRA in response to a large potassium supplement depends upon an increase in aldosterone provoked by the large dose of potassium (Miller, Waterhouse, Owens & Cohen, 1975). A supplement of 50 mmol of potas sium chloride administered to normal subjects on a zero electrolyte diet did not alter PRA (Bauer, Gauntner, Nolph & VanStone, 1977).…”

Section: Discussionmentioning

confidence: 99%

Factors Related to Potassium Transport in Chronic Stable Renal Disease in Man

et al. 1978

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1. The inter-relationships between plasma aldosterone, plasma renin activity, potassium excre tion and plasma potassium were evaluated in subjects with normal and decreased glomerular filtration rate.2. In seven studies of healthy control subjects and 12 studies of patients with renal disease, daily urine collections, plasma aldosterone and plasma renin activity were measured on a free diet for 5-^10 days and subsequently during the addition of 50 mmol of potassium chloride daily for 5 days. Plasma aldosterone was also measured in 22 hospital patients with normal glomerular filtration rate and 24 patients with reduced glomerular filtra tion rate.3. Plasma aldosterone was similar in base-line conditions in patients with or without renal disease and increased similarly during the administration of potassium chloride, suggesting that potassium excretion in patients with reduced glomerular filtra tion rate probably does not depend primarily upon increased aldosterone.4. Plasma renin activity increased similarly in control subjects and patients with renal disease during the administration of 50 mmol of potas sium chloride/day, but plasma renin activity did not increase when 100 mmol of potassium chloride/day was given to control subjects. 5. With the administration of 50 mmol of potas sium chloride/day mean daily potassium excretion Correspondence: Dr Thomas Kahn, Renal Section, D-236, Bronx Veterans Administration Hospital, 130 West Kingsbridge Road, Bronx, New York 10468, U.S.A.increased similarly in control subjects and patients with renal disease but plasma potassium increased significantly (4-7 to 5·4 mmol/1) only in patients with renal disease, suggesting that their uptake of potassium into cells was impaired.

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Section: Discussionmentioning

confidence: 99%

Factors Related to Potassium Transport in Chronic Stable Renal Disease in Man

et al. 1978

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“…61 Succinylcholine is safe in renal impairment, providing that there are no additional risk factors for succinylcholine-induced hyperkalaemia, and potassium levels are not already elevated. 62 Patients on intermittent haemodialysis often have low plasma potassium levels immediately after the completion of dialysis due to depletion of plasma potassium. Over the next few hours, intracellular potassium re-equilibrates with extracellular potassium.…”

Section: Potassiummentioning

confidence: 99%

Management of the dialysis patient in general intensive care

Arulkumaran

Montero

Singer

2012

British Journal of Anaesthesia

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The incidence of end-stage renal disease (ESRD) is rising and represents an important group of patients admitted to intensive care units (ICU). ESRD patients have significant co-morbidities and specific medical requirements. Renal replacement therapy (RRT), cardiovascular disease, disorders of electrolytes, drug metabolism, and sepsis are discussed. This review provides a practical approach to problems specific to the ESRD patient and common problems on ICU that require special consideration in ESRD patients. ESRD patients are at risk of hyperkalaemia. I.V. insulin and nebulized salbutamol lower serum potassium until definitive treatment with RRT is instituted. ESRD patients are prone to hypocalcaemia, which requires i.v. replacement if associated with complications. Midazolam has delayed metabolism and elimination in renal impairment and should be avoided. Morphine and its derivatives accumulate in renal failure and shorter-acting opiates are preferable. The use of diuretics is limited to patients with residual urine output. When required, therapeutic systemic anticoagulation should be achieved with unfractionated heparin as it is reversible and its metabolism and clearance are independent of renal function. The risk of sepsis is higher among ESRD patients when compared with patients with normal renal function. Empiric treatment should include both Gram-positive and Gram-negative cover, and methicillin-resistant Staphylococcus aureus cover if the patient has a dialysis catheter. Cardiovascular events account for the majority of deaths among ESRD patients. Troponin-I and CK-MB in combination should be used as markers of acute myocardial damage in the appropriate context, whereas B-type natriuretic peptide and troponin-T values are of less value.

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“…After a chronic increase in dietary potassium intake, a sequence of adaptive changes takes place in the kidneys that lead to the more effective and enhanced excretion of potassium after an acute potassium load (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). This response, called potassium adaptation, is associated with a sharp elevation of plasma aldosterone levels and with an increase in potassium secretion by the initial collecting, cortical collecting, and medullary collecting tubules (1-3, 11, 12, 17-21).…”

Section: Introductionmentioning

confidence: 99%

Independent effects of aldosterone and potassium on induction of potassium adaptation in rat kidney.

Stanton¹,

Pan²,

Deetjen³

et al. 1987

J. Clin. Invest.

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We examined the independent effects of a high potassium diet and increased aldosterone levels on the development of renal potassium adaptation. This condition is defined by the increased ability of the kidneys to excrete an acute infusion of potassium. Rats were adrenalectomized (ADX) and received aldosterone at basal levels (0.5 Asg/100 g * d) or at high levels (2.0 ;g/100 go d) for 10 d. In each experimental group, animals received either a control diet or a high potassium diet. In ADX animals with basal aldosterone levels, a high potassium intake increased but did not completely restore the ability to excrete potassium and induced proliferation of the basolateral membrane of principal cells in the collecting tubule (i.e, morphologic adaptation). In contrast, increased aldosterone did not induce functional adaptation. Elevated aldosterone and dietary potassium intake were required to produce functional potassium adaptation indistinguishable from that in potassium-loaded, adrenal-intact animals.

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The effect of potassium loading on sodium excretion and plasma renin activity in Addisonian man.

Cited by 19 publications

References 35 publications

Factors Related to Potassium Transport in Chronic Stable Renal Disease in Man

Factors Related to Potassium Transport in Chronic Stable Renal Disease in Man

Management of the dialysis patient in general intensive care

Independent effects of aldosterone and potassium on induction of potassium adaptation in rat kidney.

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