Dehydration and acidosis with calcification at renal tubules

Butler, Allan M.; Wilson, James L.; Farber, Sidney

doi:10.1016/s0022-3476(36)80111-5

Cited by 152 publications

(27 citation statements)

References 2 publications

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“…It is therefore biochemically characterized by failure of the kidney to produce acid urine appropriately in the presence of systemic metabolic acidosis in the setting of otherwise normal renal function and was first recognized nearly 70 yr ago (13,14). Traditionally, if the metabolic acidosis is compensated such that arterial pH is within normal limits, dRTA can be diagnosed by demonstrating failure of urinary acidification after oral ammonium chloride administration.…”

Section: Distal Rtamentioning

confidence: 99%

“…In the kidney, AE1 (kAE1) at the basolateral surface of ␣-intercalated cells is an 846 amino acid protein with multiple transmembrane spans (whether 12 or 14 has not yet been completely resolved) (25,26). It is encoded by a gene present on chromosome 17, and this same gene gives rise to an Nterminally extended 911 amino acid isoform with a separate promoter, expression of which is confined to erythrocytes (eAE1) (27).…”

Section: Autosomal Dominant Drta (Type 1a; Mim #179800)mentioning

confidence: 99%

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Inherited Distal Renal Tubular Acidosis

Karet¹

2002

Journal of the American Society of Nephrology

177

142

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Section: Distal Rtamentioning

confidence: 99%

Section: Autosomal Dominant Drta (Type 1a; Mim #179800)mentioning

confidence: 99%

Inherited Distal Renal Tubular Acidosis

Karet¹

2002

Journal of the American Society of Nephrology

177

142

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“…Chronic metabolic acidosis is associated with severe growth retardation in humans and rats (1)(2)(3)(4), and an increase in muscle protein degradation in rats (5)(6)(7). A putative causal role of metabolic acidosis in the development of whole body protein catabolism is supported by the fact that alkali-induced correction of metabolic acidosis normalized growth in children with renal tubular acidosis (4) and improved nitrogen balance significantly in acidotic patients with moderate to severe chronic renal insufficiency (8).…”

Section: Introductionmentioning

confidence: 99%

Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans.

Ballmer¹,

McNurlan²,

Hulter³

et al. 1995

J. Clin. Invest.

341

183

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Chronic metabolic acidosis has been previously shown to stimulate protein degradation. To evaluate the effects of chronic metabolic acidosis on nitrogen balance and protein synthesis we measured albumin synthesis rates and urinary nitrogen excretion in eight male subjects on a constant metabolic diet before and during two different degrees of chronic metabolic acidosis (NH4Cl 2.1 mmol/kg body weight, low dose group, and 4.2 mmol/kg body weight, high dose group, orally for 7 d). Albumin synthesis rates were measured by intravenous injection of [2H5ring]phenylalanine (43 mg/kg body weight, 7.5 atom percent and 15 atom percent, respectively) after an overnight fast. In the low dose group, fractional synthesis rates of albumin decreased from 9.9±1.0% per day in the control period to 8.4±0.7 (n.s.) in the acidosis period, and from 8.3±1.3% per day to 6.3±1.1 (P < 0.001) in the high dose group. Urinary nitrogen excretion increased significantly in the acidosis period (EA 634 mmol in the low dose group, 2,554 mmol in the high dose group). Plasma concentrations of insulin-like growth factor-I, free thyroxine and tri-iodothyronine were significantly lower during acidosis. In conclusion, chronic metabolic acidosis causes negative nitrogen balance and decreases albumin synthesis in humans. The effect on albumin synthesis may be mediated, at least in part, by a suppression of insulin-like growth factor-I, free thyroxine and tri-iodothyronine. (J. Clin. Invest. 1995. 95:39-45.) Key words: albumin * metabolic acidosis A protein synthesis * nitrogen balance * insulin-like growth factor-I

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“…In infants and children with persisting classic (Type 1) renal tubular acidosis (RTA)I (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19), the occurrence of stunted growth is characteristic (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33). In these patients, persisting acidosis might be critical to the causation of stunted growth (21-24, 27, 28, 31).…”

Section: Introductionmentioning

confidence: 99%