Sustained Metabolic Alkalosis Associated with Development of the Milk-Alkali Syndrome

Nakanishi, Takeshi; Uyama, Osamu; Yamada, Takeshi; Sugita, Minoru

doi:10.1159/000186757

Cited by 4 publications

(4 citation statements)

References 6 publications

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“…Almost all released taurine appeared in the medium on the basal side. (30) and some other tissues (17,25,28). We found that the presence of physiologic concentrations of taurine or either of the well-established MDCK cell osmolytes, (3).…”

Section: Resultsmentioning

confidence: 68%

“…taurine was identified as a major amino acid in the renal inner medulla of rats infused with 5% NaCl (30), reaching a level (65±6 mmol/kg protein) that was 40% higher than in controls. Furthermore, the same level of increased of taurine content was observed in the inner medulla when rats were prevented from drinking for 4 d. The taurine content ofthe inner medulla returned to control levels after hydration (T. Nakanishi, unpublished results).…”

Section: Introductionmentioning

confidence: 90%

See 1 more Smart Citation

Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.

Uchida¹,

Nakanishi²,

Kwon³

et al. 1991

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 90%

Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.

Uchida¹,

Nakanishi²,

Kwon³

et al. 1991

J. Clin. Invest.

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“…The expression of the carrier has been shown to be upregulated by hyperosmolality [40]. Accordingly, taurine is accumulated in rat renal medullary cells during dehydration or infusion of hypertonic saline [33], an effect paralleled by upregulation of TAUT expression in rat outer medulla [5].…”

Section: Introductionmentioning

confidence: 99%

Impaired ability to increase water excretion in mice lacking the taurine transporter gene TAUT

Huang

Boini

Lang

et al. 2005

Pflugers Arch - Eur J Physiol

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Cellular taurine uptake or release counteracts alterations of cell volume. Na+-coupled taurine transporter TAUT mediates concentrative cellular uptake of taurine. Inhibition of vasopressin secretion by hypotonicity may involve taurine release from glial cells of supraoptic nucleus. We compared renal function of mice lacking TAUT (taut-/-) and wild-type littermates (taut+/+). We observed renal taurine loss and subsequent hypotaurinemia in taut-/- mice. With free access to water, plasma and urine osmolality, urinary flow rate as well as urinary excretion and plasma concentrations of Na+ and K+ were similar in taut-/- and taut+/+ mice, whereas plasma concentrations of urea were enhanced in taut-/- mice. An oral water load (1 ml/16 g body weight) induced a similar diuresis in both genotypes. Repeating the oral water load immediately after normalization of urine flow rate, however, resulted in delayed diuresis and higher urinary vasopressin/creatinine ratios in taut-/- mice. In comparison, the repeated diuretic response to vasopressin V2 receptor blockade was not different between genotypes. Water deprivation for 36 h led to similar antidiuresis and increases of urinary osmolality in both genotypes. Upon free access to water after deprivation, taut-/- mice continued to concentrate urine up to 6 days, while taut+/+ mice rapidly returned to normal urinary osmolality. Urinary vasopressin/creatinine ratios and plasma aldosterone concentrations were not different under basal conditions but were significantly higher in taut-/- mice than in taut+/+ mice at 6 days after water deprivation. In conclusion, taut-/- mice suffer from renal taurine loss and impaired ability to lower urine osmolality and to increase urinary water excretion. The latter defect could reside extrarenally and result from a role of taurine in the suppression of vasopressin release which may be attenuated in taut-/- mice.

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“…In the present case, pre-existing renal failure attributed to long-term use of furosemide was considered Fig. 2 Histopathology of the bronchial mucosa revealed calcified lesions via H&E stain (a; arrows) and von Kossa stain (b; arrowheads), and gastric mucosa revealed calcified lesions via H&E stain (c; arrows) and von Kossa stain (d; arrowheads) responsible for the development of milk-alkali syndrome [5,6]. Furosemide inhibits the Na-K-2Cl cotransport system in the loop of Henle, reduces fluid reabsorption, and leads to hypokalemia and metabolic alkalosis.…”

Section: Discussionmentioning

confidence: 82%

Pulmonary and gastric metastatic calcification due to milk-alkali syndrome: a case report

et al. 2013

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The incidence of metastatic calcification is influenced by high serum calcium and phosphate concentrations and local physicochemical conditions, such as pH. A high pH accelerates tissue calcification. Patients with milk-alkali syndrome typically present with renal failure, hypercalcemia, and metabolic alkalosis, which are caused by the ingestion of calcium and absorbable alkali. Among patients with impairment of renal function, milk-alkali syndrome is a major cause of hypercalcemia. Long-term use of furosemide will lead to hypokalemia, metabolic alkalosis, and eventually renal failure (i.e., pseudo-Bartter syndrome). Even if the level of calcium ingestion is relatively low, the renal failure caused by long-term furosemide use can readily lead to milk-alkali syndrome. We describe a case of a 45-year-old woman who was admitted with cough and dyspnea and presented with pulmonary and gastric metastatic calcification. She had been taking alfacalcidol and oral alkaline medications such as sodium bicarbonate and calcium carbonate as well as oral furosemide for a long time. The patient was found to have hypercalcemia, chronic renal failure, and metabolic alkalosis, so milk-alkali syndrome was diagnosed. Saline was administered and oral medications were discontinued. Serum creatinine levels subsequently decreased, but pulmonary metastatic calcification was not diminished. In this case, the milk-alkali syndrome that caused the severe metastatic calcification was exacerbated by multiple factors, including oral alkaline medications such as sodium bicarbonate and calcium carbonate. In addition, metabolic alkalosis and renal failure were affected by long-term furosemide use (i.e., pseudo-Bartter syndrome).

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Sustained Metabolic Alkalosis Associated with Development of the Milk-Alkali Syndrome

Cited by 4 publications

References 6 publications

Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.

Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.

Impaired ability to increase water excretion in mice lacking the taurine transporter gene TAUT

Pulmonary and gastric metastatic calcification due to milk-alkali syndrome: a case report

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