Distal Renal Tubular Acidosis: Alkali Heals Osteomalacia and Increases Net Production of 1,25-Dihydroxyvitamin D

Wrong, Oliver; Henderson, Janet E.; Kaye, Michael P.

doi:10.1159/000087537

Cited by 10 publications

(3 citation statements)

References 40 publications

(17 reference statements)

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“…7). It is possible that these results could help to account for the osteomalacia that sometimes accompanies acidosis in renal disease [28,29,61]. …”

Section: Acidosis and Osteoblast Functionmentioning

confidence: 99%

Acid–base regulation of bone metabolism

Arnett

2007

International Congress Series

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“…7). It is possible that these results could help to account for the osteomalacia that sometimes accompanies acidosis in renal disease [28,29,61]. …”

Section: Acidosis and Osteoblast Functionmentioning

confidence: 99%

Acid–base regulation of bone metabolism

Arnett

2007

International Congress Series

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“…Serum bicarbonate values <22 mEq/L in subjects with CKD has been associated with an increased risk of fractures, because acidosis may cause dissolution of bone mineral directly through activation of osteoclasts and inhibition of osteoblast function in an attempt to restore normal acid/base balance. Additionally, metabolic acidosis has been linked to osteomalacia in patients with distal renal tubular acidosis, with healing of bone disease after alkali therapy . Other risk factors in non‐transplanted subjects include CKD itself, hypovitaminosis D, and increased bone turnover markers.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Consequences of Nephropathic Cystinosis

Florenzano

Ferreira

Nesterova

et al. 2018

Journal of Bone and Mineral Research

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Nephropathic cystinosis is a rare lysosomal storage disorder. Patients present in the first year of life with renal Fanconi syndrome that evolves to progressive chronic kidney disease (CKD). Despite the multiple risk factors for bone disease, the frequency and severity of skeletal disorders in nephropathic cystinosis have not been described. We performed systematic bone and mineral evaluations of subjects with cystinosis seen at the NIH (n = 30), including history and physical examination, serum and urine biochemistries, DXA, vertebral fracture assessment, skeletal radiographs, and renal ultrasound. Additionally, histomorphometric analyses are reported on six subjects seen at the UCLA Bone and Mineral Metabolism Clinic. In NIH subjects, mean age was 20 years (range, 5 to 44 years), 60% were CKD stages G1 to G4, and 40% had a renal transplant. Mean bone mineral density (BMD) Z-scores were decreased in the femoral neck, total hip, and 1/3 radius (p < 0.05). Low bone mass at one or more sites was present in 46% of subjects. Twenty-seven percent of subjects reported one or more long bone fractures. Thirty-two percent of subjects had incidental vertebral fractures, which were unrelated to transplant status. Long-bone deformity/bowing was present in 64%; 50% had scoliosis. Diffuse osteosclerosis was present in 21% of evaluated subjects. Risk factors included CKD, phosphate wasting, hypercalciuria, secondary hyperparathyroidism, hypovitaminosis D, male hypogonadism, metabolic acidosis, and glucocorticoid/immunosuppressive therapy. Sixty-one percent of the non-transplanted subjects had ultrasonographic evidence of nephrocalcinosis or nephrolithiasis. Histomorphometric analyses showed impaired mineralization in four of six studied subjects. We conclude that skeletal deformities, decreased bone mass, and vertebral fractures are common and relevant complications of nephropathic cystinosis, even before renal transplantation. Efforts to minimize risk factors for skeletal disease include optimizing mineral metabolism and hormonal status, combined with monitoring for nephrocalcinosis/nephrolithiasis. © 2018 This article is a U.S. Government work and is in the public domain in the USA.

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“…Citric acid, potassium citrate, sodium citrate (Polycitra; Ortho‐Mcneil‐Janssen pharmaceuticals, Inc.) are especially useful in this setting (52). Maintenance of normal serum bicarbonate with alkali therapy also raises urinary citrate, lowers the frequency of nephrolithiasis and tends to restore normal growth in children (53).…”

Section: Diagnosis and Treatment Of Type I Rtamentioning

confidence: 99%

Clinical approach to renal tubular acidosis in adult patients

Reddy

2011

International Journal of Clinical Practice

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Renal tubular acidosis (RTA) is a group of disorders observed in patients with normal anion gap metabolic acidosis. There are three major forms of RTA: A proximal (type II) RTA and two types of distal RTAs (type I and type IV). Proximal (type II) RTA originates from the inability to reabsorb bicarbonate normally in the proximal tubule. Type I RTA is associated with inability to excrete the daily acid load and may present with hyperkalaemia or hypokalaemia. The most prominent abnormality in type IV RTA is hyperkalaemia caused by hypoaldosteronism. This article extensively reviews the mechanism of hydrogen ion generation from metabolism of normal diet and various forms of RTA leading to disruptions of normal acid-base handling by the kidneys.

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Distal Renal Tubular Acidosis: Alkali Heals Osteomalacia and Increases Net Production of 1,25-Dihydroxyvitamin D

Abstract: In 2 women with distal renal tubular acidosis and osteomalacia, alkali treatment cured the bone disease and was accompanied by marked increases in the serum 1,25 dihydroxyvitamin D concentration, without a significant change in the 25-hydroxyvitamin D concentration.

Cited by 10 publications

References 40 publications

Acid–base regulation of bone metabolism

Acid–base regulation of bone metabolism

Skeletal Consequences of Nephropathic Cystinosis

Clinical approach to renal tubular acidosis in adult patients

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