Glucose modulation of the disposal of an acute potassium load in patients with end-stage renal disease

Allon, Michael; Dansby, Linda M.; Shanklin, Nancy

doi:10.1016/0002-9343(93)90081-y

Cited by 50 publications

(40 citation statements)

References 27 publications

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“…These observations in animals are in agreement with clinical studies, and show that fasting is followed by a rise in serum potassium in dialysis patients, but not in controls (50). Moreover, in hemodialysis patients, a potassium load induces an increase in plasma potassium which is greater than in controls and which is not accounted for by renal excretion (51). In postabsorptive patients studied here plasma potassium levels were directly related to forearm muscle potassium release.…”

Section: Discussionsupporting

confidence: 90%

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Garibotto¹,

Barreca²,

Russo³

et al. 1997

J. Clin. Invest.

106

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To assess the effect of recombinant human growth hormone (rhGH) on muscle protein metabolism in uremic patients with malnutrition, forearm [ 3 H]phenylalanine kinetics were evaluated in six chronically wasted (body weight 79% of ideal weight) hemodialysis (HD) patients in a self-controlled, crossover study. Forearm protein dynamics were evaluated before, after a 6-wk course of rhGH (5 mg thrice weekly) and after a 6-wk washout period. After rhGH: ( a ) forearm phenylalanine net balance-the difference between phenylalanine incorporation into and phenylalanine release from muscle proteins-decreased by 46% ( Ϫ 8 Ϯ 2 vs. Ϫ 15 Ϯ 2 nmol/min·100 ml at the baseline and Ϫ 11 Ϯ 2 after washout,

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Section: Discussionsupporting

confidence: 90%

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Garibotto¹,

Barreca²,

Russo³

et al. 1997

J. Clin. Invest.

106

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“…Gonick et al found no difference in peak S K between patients with glomerular or tubular kidney diseases or normal controls despite differences in urinary potassium excretion following potassium load of 0.75 mEq/kg (~2,050 mg potassium/70-kg person) in 8-oz of orange juice 23 . Other studies were conducted in a fasted state using lower doses of potassium (0.25 mmol/kg 24–25 and 0.5 mmol/kg 26 ), and found significantly higher peak S K in HD patients compared to controls. Importantly, fasting is known to increase S K in ESRD.…”

Section: Distribution and Excretion Of Potassium In Kidney Diseasementioning

confidence: 94%

“…Because dietary macronutrients, in particular glucose, also stimulate insulin release, they can help shift potassium intracelluarly 21–22 . The rise in S K following potassium ingestion is greatly attenuated if glucose is provided along with it 23–24 , although studies providing potassium and glucose in kidney disease patients and normal controls have produced conflicting results. Gonick et al found no difference in peak S K between patients with glomerular or tubular kidney diseases or normal controls despite differences in urinary potassium excretion following potassium load of 0.75 mEq/kg (~2,050 mg potassium/70-kg person) in 8-oz of orange juice 23 .…”

Section: Distribution and Excretion Of Potassium In Kidney Diseasementioning

confidence: 99%

Nutrient Non-equivalence: Does Restricting High-Potassium Plant Foods Help to Prevent Hyperkalemia in Hemodialysis Patients?

St-Jules

Sevick

2016

Journal of Renal Nutrition

147

129

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Hemodialysis patients are often advised to limit their intake of high-potassium foods to help manage hyperkalemia. However, the benefits of this practice are entirely theoretical and not supported by rigorous randomized controlled trials. The hypothesis that potassium restriction is useful is based on the assumption that different sources of dietary potassium are therapeutically equivalent. In fact, animal and plant sources of potassium may differ in their potential to contribute to hyperkalemia. In this commentary, we summarize the historical research basis for limiting high-potassium foods. Ultimately, we conclude that this approach is not evidence-based and may actually present harm to patients. However, given the uncertainty arising from the paucity of conclusive data, we agree that until the appropriate intervention studies are conducted, practitioners should continue to advise restriction of high-potassium foods.

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“…It has been postulated that those with diabetes are more likely to have relative aldosterone insensitivity and therefore are predisposed to the development of acidosis and hyperkalemia (31). In addition, inadequate insulin secretion may lead to extracellular potassium shifts (32). We speculate that given that this cohort of patients was being followed in nephrology clinics, concomitant diuretic use or nutritional advice to lower potassium intake may have potentially attenuated the relationship between eGFR and S K , as well as that of diabetes status and higher potassium levels, particularly among those with stages 4 to 5 CKD.…”

Section: Discussionmentioning

confidence: 99%

Serum Potassium and Outcomes in CKD

Korgaonkar¹,

Tilea²,

Gillespie³

et al. 2010

Clinical Journal of the American Society of Nephrology

197

159

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Background and objectives:The relationship between serum potassium (S K ) and mortality in chronic kidney disease (CKD) has not been systematically investigated.Design, setting, participants, & measurements: We examined the predictors and mortality association of S K in the Renal Research Institute CKD Study cohort, wherein 820 patients with CKD were prospectively followed at four US centers for an average of 2.6 years. Predictors of S K were investigated using linear and repeated measures regression models. Associations between S K and mortality, the outcomes of ESRD, and cardiovascular events in time-dependent Cox models were examined.Results: The mean age was 60.5 years, 80% were white, 90% had hypertension, 36% had diabetes, the average estimated GFR was 25.4 ml/min per 1.73 m 2 , and mean baseline S K was 4.6 mmol/L. Higher S K was associated with male gender, lower estimated GFR and serum bicarbonate, absence of diuretic and calcium channel blocker use, diabetes, and use of angiotensinconverting enzyme inhibitors and/or statins. A U-shaped relationship between S K and mortality was observed, with mortality risk significantly greater at S K <4.0 mmol/L compared with 4.0 to 5.5 mmol/L. Risk for ESRD was elevated at S K <4 mmol/L in S K categorical models. Only the composite of cardiovascular events or death as an outcome was associated with higher S K (>5.5).Conclusions: Although clinical practice usually emphasizes greater attention to elevated S K in the setting of CKD, our results suggest that patients who have CKD and low or even low-normal S K are at higher risk for dying than those with mild to moderate hyperkalemia.

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Glucose modulation of the disposal of an acute potassium load in patients with end-stage renal disease

Cited by 50 publications

References 27 publications

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Nutrient Non-equivalence: Does Restricting High-Potassium Plant Foods Help to Prevent Hyperkalemia in Hemodialysis Patients?

Serum Potassium and Outcomes in CKD

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