Renal Response to Acute Ammonium Chloride Acidosis in Subjects with Single Kidney

Chan, James C.M.; Rebecca, S.; Malekzadeh, Mohammad; Hurley, John K.; Chaimovitz, Cidio

doi:10.1016/s0022-5347(17)59956-5

Cited by 7 publications

(5 citation statements)

References 15 publications

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“…The diagnosis of classic, type I renal tubu lar acidosis was reconfirmed in each patient by the NH4CI loading test, in which the min imal urinary pH value was above 6.6 and the maximal net acid excretion was no higher than 54 pEq/min/1.73 m2, whereas the nor mal maximal net acid excretion, in relation to NH4CI loading, established in this laboratory was 97 ± 13 (iEq/min/1.73 m2 [14], The presence of hyperchloremic metabolic acido sis (tables II. Ill), the absence of azotemia (ta ble I), and the normal serum electrolytes aside from hyperchloremia (table III) were …”

Section: Clinical Datamentioning

confidence: 87%

Calcium and Hydrogen Ion Metabolism in Children with Classic (Type I/Distal) Renal Tubular Acidosis

Chan¹

1981

Ann Nutr Metab

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The rate of endogenous acid production was examined in 4 children with classic renal tubular acidosis. The interaction with calcium metabolism was studied by standard balance techniques before and after correction of metabolic acidosis with alkali solutions. The results indicate significant elevation of mean net acid production in the 4 patients (2.3 ± 0.5 mEq/kg/day) as compared to that of the 6 weight-matched normal children (1.4 ± 0.4 mEq/kg/day) (p < 0.05). This is related to elevation of urinary sulfate output. The intestinal absorption of calcium is markedly improved on correction of metabolic acidosis, which is suggestive of interference with vitamin D metabolism. It is concluded that alkali therapy exceeding the conventional 1–2 mEq/kg/day is needed to achieve optimal correction of metabolic acidosis and that the suboptimal calcium balance and increased sulfate excretion contribute to the growth failure in these subjects with renal tubular acidosis.

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Section: Clinical Datamentioning

confidence: 87%

Calcium and Hydrogen Ion Metabolism in Children with Classic (Type I/Distal) Renal Tubular Acidosis

Chan¹

1981

Ann Nutr Metab

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“…Subclinical tubular dysfunction and the presence of a single kidney to process acid loads may reduce the capacity for renal acid excretion. 1,24 Experimental studies indicate that rats with reduced nephron mass induced by subtotal nephrectomy were more susceptible to MA, which caused GFR decline mediated by endothelin. 25,26 In our study, deceased donor transplantation and tacrolimus instead of cyclosporine were also suspected to be associated with MA.…”

Section: Discussionmentioning

confidence: 99%

“…Serum sodium, potassium, chloride, TCO 2 , and creatinine values were retrospectively obtained, which were measured at 1, 3,6,9,12,18,24,36,48, and 60 months post-transplant. Serum TCO 2 was considered a surrogate measure of bicarbonate.…”

Section: Laboratory Measurementsmentioning

confidence: 99%

Metabolic Acidosis and Long-Term Clinical Outcomes in Kidney Transplant Recipients

Park¹,

Kang²,

Park³

et al. 2016

JASN

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Metabolic acidosis (MA), indicated by low serum total CO (TCO) concentration, is a risk factor for mortality and progressive renal dysfunction in CKD. However, the long-term effects of MA on kidney transplant recipients (KTRs) are unclear. We conducted a multicenter retrospective cohort study of 2318 adult KTRs, from January 1, 1997 to March 31, 2015, to evaluate the prevalence of MA and the relationships between TCO concentration and clinical outcomes. The prevalence of low TCO concentration (<22 mmol/L) began to increase in KTRs with eGFR<60 ml/min per 1.73 m and ranged from approximately 30% to 70% in KTRs with eGFR<30 ml/min per 1.73 m Multivariable Cox proportional hazards models revealed that low TCO concentration 3 months after transplant associated with increased risk of graft loss (hazard ratio [HR], 1.74%; 95% confidence interval [95% CI], 1.26 to 2.42) and death-censored graft failure (DCGF) (HR, 1.66; 95% CI, 1.14 to 2.42). Cox regression models using time-varying TCO concentration additionally demonstrated significant associations between low TCO concentration and graft loss (HR, 3.48; 95% CI, 2.47 to 4.90), mortality (HR, 3.16; 95% CI, 1.77 to 5.62), and DCGF (HR, 3.17; 95% CI, 2.12 to 4.73). Marginal structural Cox models adjusted for time-varying eGFR further verified significant hazards of low TCO concentration for graft loss, mortality, and DCGF. In conclusion, MA was frequent in KTRs despite relatively preserved renal function and may be a significant risk factor for graft failure and patient mortality, even after adjusting for eGFR.

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“…Alterations in chemical and electrical transtubular gradients, caused by increased perfusion of the transplanted kidney due to the single kidney state, could be an additional mechanism causing a decrease in NAE, as was shown for patients with nephrectomy [ 19 ].…”

Section: Kidney Transplantationmentioning

confidence: 99%

Metabolic acidosis in chronic kidney disease: mere consequence or also culprit?

Kuhn,

Mohebbi,

Ritter

2024

Pflugers Arch - Eur J Physiol

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Metabolic acidosis is a frequent complication in non-transplant chronic kidney disease (CKD) and after kidney transplantation. It occurs when net endogenous acid production exceeds net acid excretion. While nephron loss with reduced ammoniagenesis is the main cause of acid retention in non-transplant CKD patients, additional pathophysiological mechanisms are likely inflicted in kidney transplant recipients. Functional tubular damage by calcineurin inhibitors seems to play a key role causing renal tubular acidosis. Notably, experimental and clinical studies over the past decades have provided evidence that metabolic acidosis may not only be a consequence of CKD but also a driver of disease. In metabolic acidosis, activation of hormonal systems and the complement system resulting in fibrosis have been described. Further studies of changes in renal metabolism will likely contribute to a deeper understanding of the pathophysiology of metabolic acidosis in CKD. While alkali supplementation in case of reduced serum bicarbonate < 22 mmol/l has been endorsed by CKD guidelines for many years to slow renal functional decline, among other considerations, beneficial effects and thresholds for treatment have lately been under intense debate. This review article discusses this topic in light of the most recent results of trials assessing the efficacy of dietary and pharmacological interventions in CKD and kidney transplant patients.

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Renal Response to Acute Ammonium Chloride Acidosis in Subjects with Single Kidney

Cited by 7 publications

References 15 publications

Calcium and Hydrogen Ion Metabolism in Children with Classic (Type I/Distal) Renal Tubular Acidosis

Calcium and Hydrogen Ion Metabolism in Children with Classic (Type I/Distal) Renal Tubular Acidosis

Metabolic Acidosis and Long-Term Clinical Outcomes in Kidney Transplant Recipients

Metabolic acidosis in chronic kidney disease: mere consequence or also culprit?

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