The Spectrum of Endemic Renal Tubular Acidosis in the Northeast of Thailand

Abstract

We have previously reported a high prevalence of endemic renal tubular acidosis (EnRTA) in the northeast of Thailand, and our subsequent studies provided evidence that K deficiency exists in the same region. Since tubulointerstitial damage is associated with K deficiency, we postulate that this might be implicated in the pathogenesis of EnRTA and, if so, that a spectrum of tubulointerstitial abnormalities can be anticipated. In this study we evaluated renal acidification ability in 4 patients and in 11 of their relatives. We used a 3-day acid load (NH₄CI 0.1 g/kg/day) followed by 20 mg oral furosemide and monitored the maximal renal concentrating ability using water deprivation and intranasal 1-deamino-D-arginine vasopressin. The results showed that the subjects could be divided into three groups: normal relatives of the patients, those with suspected renal tubular acidosis, and patients with overt EnRTA who had chronic metabolic acidosis and a low rate of excretion of NH⁺₄. The rate of excretion of K was very low (20 ± 4 mmol/day) in patients with EnRTA and in their relatives with suspected EnRTA. The transtubular K concentration gradient was also very low in their relatives, especially in patients with suspected EnRTA (2.8 ± 0.2). With a 3-day NH₄C1 load, the rate of excretion of N⁺₄ was very low in patients with EnRTA (32 ± 9 mmol/day), and the relatives with suspected EnRTA also had a decreased capacity to excrete N⁺₄ (50 ± 14 mmol/day). In contrast, the normal relatives excreted 92 ± 12mmol of NH⁺₄/day. The patients with EnRTA could not lower their urine pH to less than 5.5 after the acid loading (6.2 ± 0.3). After furosemide (20 mg), the NH4 excretion in the patients with EnRTA was lower than in the normal relatives. Moreover, the minimum urine pH in patients with EnRTA did not fall (6.1 ± 0.2), but there was a fall to 4.8 ± 0.1 in the patients with suspected EnRTA after furosemide treatment. In conclusion, there was a spectrum of tubulointerstitial abnormalities ranging from suspected to overt distal RTA in a geographic area known to have a high prevalence of K deficiency. K deficiency might be the important pathogenetic factor of EnRTA in the northeast of Thailand.

Risk of Calcium Oxalate Nephrolithiasis after Calcium or Combined Calcium and Calcitriol Supplementation in Postmenopausal Women

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Epidemiology of pediatric urolithiasis

“…Glucose load can induce hypercalciuria, which is ascribed to decreased distal tubular calcium absorption and augmented intestinal calcium uptake. [66] High glucose can also increase the risk of urolithiasis through an increase in urinary oxalate levels. [67]…”

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Type 1 renal tubular acidosis in a patient of Type 1 diabetes mellitus: Is it coincidence or coexistence?

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