Distal tubular acidosis

Heering P, Ivens K, Aker S, Grabensee B. Distal tubular acidosis induced by FK506. Chn Transplant I998 I2(5) 465-7I. 

Ashouri OS. Hyperkalemic distal tubular acidosis and selective aldosterone deficiency combination in a patient with lead nephropathy. Arch Intern Med 1985 145 1306-1307. 

Further genes involved in other conditions responsible for renal stone development among many others could be identified e.g. osteopetrosis with tubular acidosis type 1 (xanthinoxidase), hyperoxaluria typel (alanine-glyoxylate-aminotrans-ferase), adenine-phosphoribosyltransferase deficiency (ATRTase), distal tubular acidosis and primary hypomagnesemia. 

Hy percalciaemia -Williams syndrome -Distal tubular acidosis -Hyperparathyroidism (3)... 

The normal UAG ranges from 0 to 5 mEq/L (mmol/L) and represents the presence of unmeasured urinary anions. In metabolic acidosis, the excretion of NH4+ and concurrent CP should increase markedly if renal acidification is intact. This results in UAG values from -20 to -50 mEq/L (mmol/L). This occurs because the urinary CP concentration now markedly exceeds the urinary Na+ and K+ concentrations. Diagnoses consistent with an excessively negative UAG include proximal (type 2) renal tubular acidosis, diarrhea, or administration of acetazo-lamide or hydrochloric acid (HC1). Excessively positive values of the UAG suggest a distal (type 1) renal tubular acidosis. 

Renal tubular acidosis (distal) PO 0.5-2 mEq/kg/day in 4-6 divided doses. 

One compound that has been associated with distal tubular injury is amphotericin B, a polyene antifungal agent used in the treatment of systemic mycoses caused by opportunistic fungi. Clinical utility of amphotericin B is limited by its nephrotoxicity, characterized functionally by polyuria resistant to antidiuretic hormone administration, hyposthenuria, hypokalemia, and mild 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. 

Renal tubular acidosis in liver cirrhosis is due to an inadequate concentration of sodium ions on the distal tubuli (type I). As a result, the secretion of hydrogen ions is reduced. This is attributed to cellular immune processes as well as to toxic effects such as copper or bile acids, (s. tab. 17.6)... 

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). 

Factors that regulate distal tubular secretion of are intalce of Na" and K, plasma concentration of mineralocor-ticoids, and acid-base balance. Because renal conservation mechanisms are slow to respond, depletion can be an early consequence of restricted intake or losses of K by extrarenal routes. Diminished glomerular filtration rate is typical of renal failure, and the consequent decrease in distal tubular flow rate is an important factor in the retention of K seen in chronic renal failure. Renal tubular acidosis and metaboUc and respiratory acidoses and alkaloses also affect renal regulation of excretion. These topics are discussed in much greater detail in Chapters 45 and 46. 

The common N-terminal explains the ability of PTHrP to interact with the PTH/PTHrP receptor, mimicking the biological actions of PTH in classic target tissues, including bone and kidney. Like PTH, PTHrP causes hypercalcemia and hypophosphatemia t and increases urinary cyclic AMP. However, when compared with patients with primary hyperparathyroidism, patients with PTHrP-induced hypercalcemia have lower concentrations of l,25(OH)2D and more typically have metabolic alkalosis (instead of hyperchloremic metabolic acidosis), reduced distal tubular calcium reabsorption, and reduced and uncoupled bone formation. 

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