Spontaneous Remission of the Defect in Urinary Acidification After Cadaver Kidney Homotransplantation

Better, Ori S.; Chaimowitz, C.; Alroy, G; Sisman, I.

doi:10.1016/s0140-6736(70)90464-2

Cited by 33 publications

(18 citation statements)

References 3 publications

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“…This finding is compatible with that of Better et al [2,3]. The present studies extend the observations of Better et al [3] and demonstrate an acidification defect in live-related kidney allografts.…”

Section: Discussionsupporting

confidence: 94%

“…Previous studies have indicated that cadaveric renal allografts fail to respond adequately to an ammonium chloride load when compared with allografts from normal adults [2,3,11]. This defective renal acidification has been ascribed to severe acute tubular necrosis sustained at the time of transplantation, to rejection (acute and chronic), and to incomplete renal tubular acidosis [2,3,11].…”

Section: Introductionmentioning

confidence: 99%

“…This defective renal acidification has been ascribed to severe acute tubular necrosis sustained at the time of transplantation, to rejection (acute and chronic), and to incomplete renal tubular acidosis [2,3,11].…”

Section: Introductionmentioning

confidence: 99%

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The Adaptation of Hydrogen Ion Excretion Associated with Nephron Reduction in Post-transplant Patients

et al. 1973

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ExtractThe compensatory growth of the single and transplanted kidney is demonstrated by the improvement of glomerular filtration rate (GFR) of the single kidney to achieve 50-90% of the normal value. The compensatory renal tubular acid excretion is also studied. It is clearly demonstrated that in response to a standard ammonium chloride load (75 mEq/m 2 ) systemic acidosis (tCO 2 < 16 mEq/liter) occurs uniformly at 300^4-00 min but maximal renal acid excretion (98 ± 12 and 76 ± 17 yuEq/min/ 1.73 m 2 ) occurs in the normal and single kidney subjects, respectively, at 300-400 min, whereas, for the transplant subjects, maximal acidifications of 72 ± 34 and 74 ± 26 juEq/min/1.73 m 2 are achieved at 800 and 1,400 min for live-related and cadaveric allografts, respectively. The slower and suboptimal renal response accounts for the persistence of metabolic acidosis in the transplant population.The studies document that the important limiting factor is the reduction in glomerular filtration rate in the transplant subjects. When the low net acid excretion in the two transplant groups are factored by GFR, they become comparable with the control (donor) group as well as the normal group (P > 0.95), i.e., each remaining nephron is excreting acid normally (or supernormally) and is supportive of the "intact nephron" hypothesis.The data show a marked difference in urinary pH during acidosis between the two transplant groups: 50% of the cadaveric allografts have an inability to lower urine pH below 5.4 compared with 10% only of the live-related allografts which show such a defect. This would imply that cadaver allografts are more susceptible to an acute acid load. SpeculationThe ischemia sustained at the time of transplantation results in acute tubular damage and proportionate lowering of the glomerular filtration rate which account for the impaired acidification capacity in the kidney allografts. It is also possible that circulatory damage to the glomeruli may occur in the transplantation process. It is even possible that intrarenal circulation may be altered by either transplantation or nephrectomy; although, admittedly, this last possibility seems quite unlikely. It is open to speculation what effect the age difference between the donors and the recipients may have on their different responses to acute metabolic acidosis. 712Adaptation of hydrogen ion excretion 713

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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The Adaptation of Hydrogen Ion Excretion Associated with Nephron Reduction in Post-transplant Patients

et al. 1973

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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%

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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“…Several authors have noticed reduced urinary excretion of ammonium relative to renal functional mass, and to the ability to lower urinary pH [8][9][10], This may result from severe malnutrition [27], or protein restriction during the time prior to transplantation. It may also be caused by a specific defect in production of ammonium.…”

Section: Ammonium Excretionmentioning

confidence: 99%

Tubular Dysfunction following Kidney Transplantation

Better¹

1980

Nephron

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Spontaneous Remission of the Defect in Urinary Acidification After Cadaver Kidney Homotransplantation

Cited by 33 publications

References 3 publications

The Adaptation of Hydrogen Ion Excretion Associated with Nephron Reduction in Post-transplant Patients

The Adaptation of Hydrogen Ion Excretion Associated with Nephron Reduction in Post-transplant Patients

Dietary Acid Load and Metabolic Acidosis in Renal Transplant Recipients

Tubular Dysfunction following Kidney Transplantation

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