Renal tubular acidosis, acidosis due to hyperkalemia, hypercalcemia, disordered citrate metabolism and other tubular dysfunctions following human renal transplantation

Györy, Á. Z.; Stewart, John H.; George, C. R. P.; Tiller, D. J.; Edwards, K. D. G.

doi:10.1097/00007890-197004000-00011

Cited by 14 publications

(23 citation statements)

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“…Type 1 classic distal RTA has been reported more frequently in kidney recipients. 2,3,5,[8][9][10] Similarly, in this study, we observed that the presence of distal RTA was higher compared with other types of RTA.…”

Section: Discussionsupporting

confidence: 79%

Renal tubular acidosis in renal transplantation recipients

et al. 2010

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Aim: We aimed to investigate the prevalence, type, and possible risk factors of renal tubular acidosis (RTA) in Turkish patients with renal transplantation. Patients and method: The study included 66 adult renal transplantation recipients. We recorded the parameters of venous blood gas analysis including serum pH value, serum bicarbonate (HCO 3 ) concentration, presence of metabolic acidosis, which was defined as low HCO 3 (<22 mEq/L), and serum pH value (<7.35) together, and base excess and urine pH at the last follow-up. Creatinine clearance was determined from 24-hour collected urine samples. RTA was defined to be metabolic acidosis with normal serum anion gap and positive urine anion gap. Results: Mean age of 66 patients was 37.0 ± 10.4 years; 48 of 66 patients were male. RTA was found in 14 (21.2%) patients. Considering for differential diagnosis of RTA, 4 patients had type 2 RTA and 10 had type 1 RTA. On the contrary, type 4 RTA was observed in no patients. Creatinine clearance was meaningfully lower in acidosis group than in those of the nonacidosis group (55.16 ± 23.27 vs. 71.06 ± 28.14 mL/min; p = 0.028). HCO 3 was correlated with hemoglobin level (r = 0.423, p = 0.001) and creatinine clearance (r = 0.262, p = 0.034). It was inversely correlated with cyclosporine A (CsA) level (r = −0.499, p = 0.035). Conclusion: RTA is a common complication after kidney transplantation. It is related with low creatinine clearance, low hemoglobin level, and high CsA level. Particularly, the value of creatinine clearance is lower and the possibility of RTA is higher.

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Section: Discussionsupporting

confidence: 79%

Renal tubular acidosis in renal transplantation recipients

et al. 2010

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“…Since marked alkalosis accompanied the hypokalemic states in the present study, and conversely both patients presented with a slight acidosis after dietary potassium supplements, the remarkable change of renal bicarbonate threshold despite a moderate increase of extracellular potassium concentration might therefore be explained on the basis of the observations of Grantham et al In contrast to our studies in hypokalemic states, hyperkalemia has been shown experimentally to cause renal tubular acidosis as a result of a bicarbonate wasting syndrome [6]. Hyperkalemia following human renal transplantation induces acidosis [8]. Edelmann [5] has observed a patient with hyperkalemia and renal tubular acidosis.…”

Section: Discussioncontrasting

confidence: 67%

Hypokalemia, a Factor Influencing Renal Bicarbonate Reabsorption: Continued Studies on the Regulatory Mechanisms Governing Renal Handling of Acid-Base in Children

et al. 1971

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ExtractIn a program concerned with regulatory mechanisms influencing the renal contribution to acid-base balance in pediatric-aged subjects, two patients with hypokalemic alkalosis were studied. The relation of scrum potassium level to proximal tubular bicarbonate reabsorption was assessed at different potassium levels during states of equal plasma volumes or equal extracellular fluid (ECF) volumes. Renal bicarbonate threshold was cither determined by means of bicarbonate titration studies or estimated from urinary pH and simultaneous plasma bicarbonate concentration. Estimation of threshold was judged to be acceptable if pH values in urine were close to 6.2, thereby indicating little or no spilling of bicarbonate into the urine. Simultaneous plasma bicarbonate concentrations indicated renal bicarbonate threshold.Patient NAI exhibited a renal bicarbonate threshold of 25 mmoles/liter at a serum potassium level of 1.7 mval/liter and 20.5 mmoles/liter at a potassium level of 2.7 mval/liter. Plasma volume was 54.7 and 52.9 ml/kg body weight, respectively.Patient BE showed a renal bicarbonate threshold of 24.3 mmoles/liter with an ECF volume of 474 ml/kg body weight and a serum potassium level of 1.7 mval/ liter; however, this patient exhibited a renal bicarbonate threshold of less than 21 mmoles/liter with an ECF volume of 454 ml/kg body weight and a potassium level of 3.2 mval/liter.In both patients, renal bicarbonate threshold decreased when serum potassium levels increased. Moreover, plasma volume in one patient and ECF volume in the other either had decreased slightly or had remained essentially unchanged. Hence, an indirect relation was found between serum potassium level and renal bicarbonate threshold. Plasma volume, known to influence renal bicarbonate threshold, was without effect on this relation. SpeculationIn hypokalemic alkalosis the level of serum potassium itself or the levels of serum potassium as indicators of whole body potassium might be among the factors influencing renal bicarbonate reabsorption. 618Hypokalemia and renal bicarbonate reabsorption 619

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“…Acidosis has long been recognized as a risk factor in RTRs, and several potential causes have been suggested (26)(27)(28)(29)(30). Well known contributors to acidosis are reduced nephron mass, resulting in decreased acid excretion, and use of pharmacologic agents, such as calcineurin inhibitors, that directly influence acid-base status but also play a significant role in renal acid handling.…”

Section: Discussionmentioning

confidence: 99%

“…Body mass index was 26 (Table 1). NAE was positively associated with eGFR; use of mycophenolate; serum chloride; and urinary excretion of ammonia, TA, phosphorus, and sulfate.…”

Section: Patient Characteristicsmentioning

confidence: 99%

Dietary Acid Load and Metabolic Acidosis in Renal Transplant Recipients

Berg

Engberink

Brink

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Acidosis is prevalent among renal transplant recipients (RTRs) and adversely affects cardiometabolic processes. Factors contributing to acidosis are graft dysfunction and immunosuppressive drugs. Little is known about the potential influence of diet on acidosis in RTRs. This study examined the association of metabolic acid load with acidosis and with cardiovascular risk factors in RTRs and aimed to identify dietary factors associated with acidosis.Design, participants, setting, & measurements 707 RTRs were included. Metabolic acid load was assessed by measuring 24-hour urinary net acid excretion (NAE; i.e., titratable acid + ammonium 2 bicarbonate). Acidosis was defined as serum [HCO 3 2 ] , 24 mmol/L. BP and insulin resistance, reflected by hemoglobin A1c, were among cardiovascular risk factors. Diet was assessed with food-frequency questionnaires. Linear regression analysis was applied to investigate association between NAE and acidosis and between dietary factors and acidosis.Results Mean age 6 SD was 53613 years; 57% of patients were male. Acidosis was present in 31% of RTRs. NAE was associated with acidosis (serum HCO 3 2 : b=20.61; serum pH: b=20.010; both P,0.001). Patients with high intake of animal protein (i.e., from meat, cheese, and fish) and low intake of fruits and vegetables had significantly lower serum HCO 3 2 and serum pH. No associations were observed between NAE and cardiovascular risk factors, such as hypertension and insulin resistance.Conclusions In addition to conventional factors contributing to acidosis, diet might influence acid-base homeostasis in RTRs. Higher intake of fruits and vegetables and lower animal protein intake is associated with less acidosis in RTRs.

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Renal tubular acidosis, acidosis due to hyperkalemia, hypercalcemia, disordered citrate metabolism and other tubular dysfunctions following human renal transplantation

Cited by 14 publications

References 0 publications

Renal tubular acidosis in renal transplantation recipients

Renal tubular acidosis in renal transplantation recipients

Hypokalemia, a Factor Influencing Renal Bicarbonate Reabsorption: Continued Studies on the Regulatory Mechanisms Governing Renal Handling of Acid-Base in Children

Dietary Acid Load and Metabolic Acidosis in Renal Transplant Recipients

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