Incomplete Renal Tubular Acidosis Research Articles

Central, renal and adrenal effects of lithium in man

The effect of lithium on thirst and plasma vasopressin concentration was tested in seven subjects with affective psychiatric disorders. Mean ad libitum fluid intake was liberal but no different before (3,293 ml/day) and three to four weeks after treatment with lithium (3,443 ml/day). After fluid deprivation, plasma vasopressin was 1.5 ± 0.39 pg/ml before and 3.72 ± 0.55 pg/ml after treatment with lithium (p < 0.02) as plasma osmolalities and body weights were comparable. Urinary osmolalities were no different (735 versus 759 mOsm/kg) and did riot increase with exogenous vasopressin. With a water load, plasma vasopressin decreased 1.58 to 0.79 pg/ml (p < 0.05) before and from 2.68 to 0.91 pg/ml (p < 0.025) after treatment with lithium. The water load excreted in 4 hours was less during lithium therapy (66 versus 85 per cent, p < 0.05). Lithium therapy had no effect on plasma renin activity (PRA) or aldosterone. On standing, PRA increased from 2.27 to 5.28 ng/ml/hour (p < 0.05) before and from 2.19 to 7.59 ng/ ml/hour (p < 0.05) after lithium therapy. At the same time plasma aldosterone increased from 121 to 365 pg/ml (p < 0.05) before and from 76 to 436 pg/ml (p < 0.05) after treatment with lithium. Lithium had no effect on indices of proximal tubular function (HCO 3 −, HPO 4 =, glucose, amino acid and uric acid excretion). A lower titratable acid excretion (21 ± 5 versus 32 ± 4 μeq/min, p < 0.05) and higher urine pH (5.40 versus 5.02, p < 0.05) was observed after NH 4Cl ingestion during lithium therapy as compared to control. In conclusion, three to four weeks of lithium therapy neither stimulates thirst nor suppresses vasopressin release; some of the polyuria in patients with affective disorders may be due to their liberal fluid intakes. Lithium does not alter base line or standing PRA, aldosterone or proximal tubular function. Lithium does, however, induce an incomplete renal tubular acidosis.

Incomplete Distal Renal Tubular Acidosis in Hypomagnesemia-Dependent Hypocalcemia

The mechanism perpetuating hypocalcemia in the presence of hypomagnesemia is unknown. Two patients with this disorder had elevated immunoreactive serum parathyroid hormone levels and incomplete distal renal tubular acidosis. All abnormalities were corrected with magnesium replenishment. Postulated mechanisms include (1) parathyroid hormone activation in the serum or at the site of action dependent on magnesium, and (2) abnormalities in vitamin D metabolism that can be corrected by magnesium replacement.

Incomplete Renal Tubular Acidosis: some Clinical and Physiological Features

17 patients with recurrent calcium-containing renal calculi were studied using the short NH4Cl test and one subject with 'incomplete renal tubular acidosis' was identified. In retrospect the only clue to this diagnosis was a fasting, morning urine pH exceeding 6.0 units. Fasting morning urine pH, which is usually less than 6.0 in subjects who acidify normally, is proposed as a simple screening test for 'incomplete RTA'. Modified high dose NH4Cl tests and Na2SO4 tests were performed in this subject and other patients with either complete or incomplete distal renal tubular acidosis. These studies suggest that the ability to lower urine pH is impaired less with the incomplete than with the complete form of the disease.

Hypercalcaemia, hypophosphataemia, and inability to excrete hydrogen ions.

Investigation of a patient with hypercalcaemia, hypophosphataemia, and nephrocalcinosis failed to lead to a clear diagnosis. Neither primary hyperparathyroidism nor primary incomplete renal tubular acidosis could explain all the biochemical features, and it seems that more than one fundamental abnormality may have been present.

Incomplete renal tubular acidosis in sickle cell disease

To evaluate renal acidification capacity in sickle cell nephropathy 6 subjects with sickle cell trait (Hb AS), 8 patients with sickle cell hemoglobin C disease (Hb SC), 13 with homozygote sickle cell anemia (Hb SS) and 7 normal controls (Hb AA) were submitted to Wrong and Davies' acidification test. Renal concentrating capacity and glomerular filtration rate were also estimated. Urinary pH after acid loading was significantly higher, titratable acidity (TA) significantly lower in SC and SS patients compared to AS subjects and normals. NH 4 + excretion did not differ between the four groups. In none of the subjects investigated was metabolic acidosis found, characterizing the acidification defect in sickle cell nephropathy as the incomplete form of renal tubular acidosis (RTA). A correlation between the degree of disturbance in renal acidifying and concentrating capacity could be observed.

Urinary Calculi Associated with Incomplete Renal Tubular Acidosis

No AccessJournal of Urology1 Feb 1972Urinary Calculi Associated with Incomplete Renal Tubular Acidosis J.D. Young, and Luis G. Martin J.D. YoungJ.D. Young More articles by this author , and Luis G. MartinLuis G. Martin More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)60975-3AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1972 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited ByKumagai I, Matsuo S and Kato T (2018) A Case of Incomplete Renal Tubular Acidosis (Type 1) Associated with Medullary Sponge Kidney Followed By NephrocalcinosisJournal of Urology, VOL. 123, NO. 2, (250-252), Online publication date: 1-Feb-1980. Volume 107Issue 2February 1972Page: 170-173 Advertisement Copyright & Permissions© 1972 by The American Urological Association Education and Research, Inc.MetricsAuthor Information J.D. Young More articles by this author Luis G. Martin More articles by this author Expand All Advertisement Loading ...

Studies on acid excretion in adults with sickle-cell anaemia.

1. The acid excretion of patients with sickle-cell anaemia has been studied. 2. There is a mild defect in urinary acidification and a decreased H+ excretion in response to ammonium chloride loading. 3. The acidification defect was not corrected by oral administration of a phosphate solution. 4. Infusion of a sodium sulphate solution in subjects who were avidly reabsorbing sodium produced equal degrees of urine acidification in patients and controls. 5. Studies on bicarbonate reabsorption were inconclusive. 6. We conclude that patients with sickle-cell anaemia have a mild form of incomplete distal renal tubular acidosis.

Renal Tubular Acidosis Due to Amphotericin B Nephrotoxicity

Urinary acidification after ammonium chloride loading was evaluated in 22 patients treated with amphotericin B and in ten normal volunteers. Six patients were studied while receiving amphotericin B; all had defective renal excretion of acid, although systemic acidosis was absent. Four of these patients were restudied following treatment; three were normal at two, four, and eight months respectively; and one remained abnormal at ten months. Three patients, initially studied one to five months after completion of treatment, excreted an acid load normally. Fourteen patients studied more than a year following treatment with amphotericin B were all normal. Incomplete renal tubular acidosis is a common, but reversible, complication of amphotericin B therapy. Urinary acidification is normal within a few months after treatment is discontinued. Alkali therapy is indicated in patients who develop renal tubular acidosis and potassium supplementation should be given if hypokalemia appears.

Hypokalemic Rhabdomyolysis and Myoglobinuria Following Amphotericin B Therapy

Amphotericin B-induced hypokalemia progressed to profound muscle weakness, rhabdomyolysis, and myoglobinuria in a patient with cryptococcal meningitis. Incomplete renal tubular acidosis which was present during therapy may have predisposed the patient to renal potassium wasting.

Syndrome of incomplete renal tubular acidosis after cadaver kidney transplantation.

Renal capacity to excrete acid and lower urinary pH was tested nine patients after cadaver kidney homotransplantation by the short, oral ammonium chloride loading test of Wrong and Davies. The control population consisted of 15 healthy subjects. The patients had a defect in acid excretion resembling incomplete renal tubular acidosis. This defect could not be accounted for by the moderate reduction in glomerular filtration rate. Impaired ability to dilute and concentrate the urine was also shown in the patients. The presence of these abnormalities suggested the occurrence of distal tubular dysfunction in the kidneys transplanted from cadavers. On the basis of these findings it is proposed that the defect in renal acid excretion contributes to the genesis of the metabolic acidosis that occasionally complicates rejection episodes in such patients.

Incomplete renal tubular acidosis: Physiologic studies in three patients with a defect in lowering urine pH

A defect in ability to lower urine pH in response to ammonium chloride loading in the absence of systemic acidosis is defined as the syndrome of incomplete renal tubular acidosis. Three patients are described who had recurrent nephrolithiasis in association with incomplete renal tubular acidosis. Two of these had hypercalciuria, one of whom had nephrocalcinosis. The third patient had nephrocalcinosis without hypercalciuria. All patients had low urinary citrate levels. Two had defects of the renal concentrating mechanism, one of whom had potassium depletion. In one patient classic renal tubular acidosis subsequently developed. The ability to lower urine pH was tested by acute and chronic ammonium chloride loading and by sodium sulfate infusion. In two patients minimum urine pH after sodium sulfate infusion was approximately 1 pH unit lower than after ammonium chloride loading. In one patient sodium restriction prior to acute ammonium chloride loading interfered with the patient's ability to lower urine pH. A possible mechanism for the defect in ability to generate a steep blood-to-urine hydrogen ion gradient in patients with renal tubular acidosis is suggested.

Multiple renal tubular defects. Report of a case with vasopressin-resistant polyuria, amino-aciduria and incomplete renal tubular acidosis.

With an increasing understanding of normal and abnormal renal tubular function during the past several years, a wide spectrum of tubular transport defects have been described. These may occur singly as in renal glycosuria, vitamin D-resistant rickets, and nephrogenic diabetes insipidus, or they may present as multiple defects as in the Fanconi syndrome with glycosuria, phosphaturia and amino-aciduria. 1 Many of the tubular defects in this spectrum of disorders are poorly understood and therefore not clearly defined. The case cited below presented with polyuria as his only symptom of renal tubular dysfunction, but after several studies were performed he was found to have not only vasopressin-resistant diabetes insipidus but also amino-aciduria and incomplete renal tubular acidosis. It is of interest that the patient's disorder was not recognized until he was 54 years of age, even though the abnormalities were probably present since childhood. Report of Case First Admission.— A 54-year-old