Distal renal tubular acidosis

Incomplete distal renal tubular acidosis has been attributed to lithium, but appears to be of no clinical significance (400). 

Carlisle EJ, Donnelly SM, Vasuvattakul S, Kamel KS, Tobe S, Halperin ML. Glue-sniffing and distal renal tubular acidosis sticking to the facts. J Am Soc Nephrol 1991 l(8) 1019-27. 

Moss AH, Gabow PA, Kaehny WD, Goodman SI, Haut LL. Fanconi s syndrome and distal renal tubular acidosis after glue sniffing. Ann Intern Med 1980 92(l) 69-70. 

A 25-year-old woman developed biopsy-proven chronic tubulointerstitial nephritis with accompanying distal renal tubular acidosis in association with furosemide abuse (up to 1.2 g/day for several months) (9). 

Park CW, You HY, Kim YK, Chang YS, Shin YS, Hong CK, Kim YC, Bang BK. Chronic tubulointerstitial nephritis and distal renal tubular acidosis in a patient with frusemide abuse. Nephrol Dial Transplant 2001 16(4) 867-9. 

Ammonium chloride, bicarbonate, and furosemide loading tests in an epileptic man with metabolic acidosis and episodic hypokalemia taking zonisamide showed evidence of distal renal tubular acidosis (9). On reexamination 7 weeks after zonisamide had been replaced with phenytoin, the renal tubular acidosis had resolved. 

Nephrogenic diabetes insipidus has been described in patients receiving foscarnet, either alone or associated with a distal renal tubular acidosis [66, 67, 68]. In fact, a recent review cited foscarnet as the second most common reported cause of drug-induced diabetes insipidus, second only to lithium [69]. In experiments using toad urinary bladders [70], serosal application of foscarnet enhanced water flow in the presence of submaximal ADH concentrations, but did not affect water transport in the absence of ADH or when maximal concentrations of ADH were used. Mucosal foscarnet did not affect water transport. Further studies are needed to clarify the mechanisms for altered water handling by the kidneys with foscarnet. 

Eiam-Ong B, Dafnis E, Spohn M, Kurtzman NA, Sabatini S. H/K/ATpase in distal renal tubular acidosis urinary tract obstraction, lithium, and amiloride. Am J Physiol 1993 265 (6Pt2) F675-F680. 

Domrongkitchaipom S, Khositseth S, Stitchantrokul W, et al. Dosage of potassium citrate in the correction of urinary abnormalities in pediatric distal renal tubular acidosis patients. Am Kidney Dis 2002 39(2) 383-391. 

A 36-year-old patient started taking a combination of herbal products including Echinacea, and 2 weeks later she presented with generalized muscle weakness that limited her ambulation and ability to use her hands. She was found to have distal renal tubular acidosis and was extremely hypokalemic (K+ of 1.3). Over 4 days she received 1200 mEq of sodium bicarbonate and 400 mEq of potassium chloride along with other electrolyte supplements to correct the imbalances. After her serum electrolytes were corrected, her muscle weakness improved rapidly. She was diagnosed and treated for Sjogren s syndrome and her condition rapidly improved. The researchers suggested that her use of the immunostimulant Echinacea could have contributed to the activation of her autoimmune disease, which ultimately caused her severe metabolic disturbances. Because she had remained symptom free for more than 3 years, the authors concluded that, after review, her disease was relatively mild and was exacerbated by Echinacea (34). 

Toxicity is often initially manifest by abnormahties of renal tubular function including potassium, sodium, and magnesium wasting, impaired urine concentrating ability, and distal renal tubular acidosis due to a leak of hydrogen ions back out of the tubular lumen. Substantial potassium and magnesium replacement may be necessary. Renal blood flow and GFR decreases are common, and result in a rise in serum creatinine and blood urea nitrogen concentrations. 

Other chronic disorders cause osteomalacia. " " Phosphate depletion from low dietary intake, phosphate-binding antacids, and oncogenic osteomalacia (potentially phosphaturic effect) can cause osteomalacia. Hypophosphatasia is an inborn error of metabolism in which deficient activity of alkaline phosphatase causes impaired mineralization of bone matrix. Acidosis from renal dysfunction, distal renal tubular acidosis, hypergammaglobulinemic states (e.g., multiple myeloma), and drugs (e.g., chemotherapy) compromises bone mineralization. Renal tubular disorders secondary to Fanconi s syndrome, hereditary diseases (e.g., Wilson s disease, a defect in copper metabolism), acquired disease (e.g., myeloma), and toxins (e.g., lead) cause osteomalacia to varying degrees. Chronic wastage of phosphorus and/or calcium limits mineralization, which may be further compromised by acidosis and secondary hyperparathyroidism. 

Bergman, A.J., Donckerwolcke, R.A., Duran, M., Smeitink, J.A., Mousson, B., Vianey-Saban, C. Poll-The, B.T. (1994). Pediatr Res 36 582-588. Rate-dependent distal renal tubular acidosis and carnitine palmitoyltransferase 1 deficiency. 

Urinary tract The susceptibUity factors for topiramate-induced renal stones have been studied in six subjects [321. After 5 days treatment there was a 31% reduction in mean calcium and a 40% reduction in mean citrate urinary concentrations. Dose escalation was associated with a further reduction in citrate concentration. The authors concluded that topiramate causes a profound reduction in urinary citrate concentrations, equivalent to the changes seen in distal renal tubular acidosis. 

Metabolism A 47-year-old woman developed a severe metabolic acidosis with a raised anion gap [100" ]. She had a chronic distal renal tubular acidosis, which was attributed to chronic toluene toxicity secondary to paint thinner and spray paint inhalation. 

Cystinuria may serve as an example of a hereditary aminoaciduria leading to urolithiasis. Bartter s syndrome and distal renal tubular acidosis (d-RTA) are disorders mostly characterised by nephrocalcinosis. The severe polyuria of nephrogenic diabetes insipidus may cause impressive dilatation of the upper urinary tract similar to urinary obstruction... 

Medullary NC and calcium phosphate stones are common in patients with distal renal tubular acidosis (dRTA) (Fig. 20.4) (Buckalew 1989 Guckel et al. 1989). A high urinary pH, hypercalciuria, and hypocitraturia contribute to these findings (Hamm 1990). In the complete form of dRTA the urine pH cannot be lowered to less than 6.1 after an acid loading test (Hesse and Vahlensieck 1986). 

Preminger GM, Sakhaee K, Skurla C, Pak CYC (1985) Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis. J Urol 134 20-24... 

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