Renal Insufficiency and Severe Calcinosis Due to Excessive Alkali‐Intake

Holten, C; Lundbæk, K

doi:10.1111/j.0954-6820.1955.tb10281.x

Cited by 13 publications

(2 citation statements)

References 4 publications

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“…Burnett and Commons [15] reported nephrocalcinosis from a single autopsy. Other autopsy reports described parietal to complete glomerulus hyalinization, thickening of Bowman's capsule, tubular atrophy and diffuse lymphocytic infiltration [16][17][18]. Extensive calcification of convoluted renal tubular cells and the tubular lamina was described as a striking feature [11].…”

Section: Renal Outcomementioning

confidence: 98%

Renal Injury in Calcium-Alkali Syndrome

Morishita¹

2012

J Nephrol Therapeutic

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Calcium-alkali syndrome is characterized by hypercalcemia, renal injury and metabolic alkalosis. Calcium-alkali syndrome caused by calcium carbonate and vitamin D has been increasing in association with their growing use for the treatment and prevention of osteoporosis. Renal injury is the most critical factor determining the severity and prognosis of this syndrome. This review focuses on the mechanism and clinical aspects of renal injury in calcium-alkali syndrome.

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Section: Renal Outcomementioning

confidence: 98%

Renal Injury in Calcium-Alkali Syndrome

Morishita¹

2012

J Nephrol Therapeutic

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“…Other autopsy reports described partial to complete glomerulus hyalinization, thickening of the Bowman capsule, tubular atrophy, vascular changes, and diffuse lymphocytic infiltration. [68][69][70] Extensive calcification of convoluted renal tubular cells and the tubular lamina was described as a striking feature. 68 Scholz and Keating 10 reported a case of focal calcification in the renal tubules that was apparent on a kidney biopsy specimen from a patient with MAS.…”

Section: Histologic Findingsmentioning

confidence: 99%

Milk-Alkali Syndrome

Medarov

2009

Mayo Clinic Proceedings

107

113

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Milk-alkali syndrome (MAS) consists of hypercalcemia, various degrees of renal failure, and metabolic alkalosis due to ingestion of large amounts of calcium and absorbable alkali. This syndrome was first identified after medical treatment of peptic ulcer disease with milk and alkali was widely adopted at the beginning of the 20th century. With the introduction of histamine2 blockers and proton pump inhibitors, the occurrence of MAS became rare; however, a resurgence of MAS has been witnessed because of the wide availability and increasing use of calcium carbonate, mostly for osteoporosis prevention. The aim of this review was to determine the incidence, pathogenesis, histologic findings, diagnosis, and clinical course of MAS. A MEDLINE search was performed with the keyword milk-alkali syndrome using the PubMed search engine. All relevant English language articles were reviewed. The exact pathomechanism of MAS remains uncertain, but a unique interplay between hypercalcemia and alkalosis in the kidneys seems to lead to a self-reinforcing cycle, resulting in the clinical picture of MAS. Treatment is supportive and involves hydration and withdrawal of the offending agents. Physicians and the public need to be aware of the potential adverse effects of ingesting excessive amounts of calcium carbonate.

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