Reversible Renal Failure Caused by Hypercalcemia

Lins, Lars‐Eric

doi:10.1111/j.0954-6820.1978.tb14879.x

Cited by 43 publications

(16 citation statements)

References 25 publications

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“…Fourth, this patient suffered acute-on-chronic renal failure, most likely due to hypercalcaemia (peaking at more than 17.0 mg/dL). Serum calcium concentrations from 12.0 to 15.0 mg/dL have been shown to decrease GFR by direct vasoconstriction and natriuresis leading to volume depletion and pre-renal azotemia [ 16 ]. Additionally, aquaporin-2 downregulation along with tubulointerstitial injury resulting in impaired osmotic gradient formation may preclude effective urine concentrating mechanisms [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

Hyperparathyroidism with hypercalcaemia in chronic kidney disease: primary or tertiary?

Lunn

Mendoza

Pasche

et al. 2010

Clinical Kidney Journal

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Objective. This study aims to highlight the challenges in the diagnosis of hyperparathyroidism (HPT) in patients with advanced chronic kidney disease (CKD).Methods. In this report, we describe a middle-aged Filipino gentleman with underlying CKD who presented with intractable nausea, vomiting, severe and medically refractory hypercalcaemia and parathyroid hormone (PTH) concentrations in excess of 2400 pg/mL. The underlying pathophysiology as well as the aetiologies and current relevant literature are discussed. We also suggest an appropriate diagnostic approach to identify and promptly treat patients with CKD, HPT and hypercalcaemia.Results. Evaluation confirmed the presence of a large parathyroid adenoma; HPT and hypercalcaemia resolved rapidly following resection.Conclusion. This case report is remarkable for its severe hypercalcaemia requiring haemodialysis, large adenoma size, acute-on-chronic kidney injury and markedly elevated PTH concentration in association with primary HPT in CKD.

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Section: Discussionmentioning

confidence: 99%

Hyperparathyroidism with hypercalcaemia in chronic kidney disease: primary or tertiary?

Lunn

Mendoza

Pasche

et al. 2010

Clinical Kidney Journal

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“…Renal manifestations of hypercalcemia consist of nephrogenic diabetes insipidus with resultant polyuria, renal vasoconstriction, distal renal tubular acidosis, and in more chronic cases, nephrolithiasis, tubular dysfunction, and chronic renal failure. [ 28 29 ]…”

Section: Clinical Presentation Of Hypercalcemiamentioning

confidence: 99%

Hypercalcemia of malignancy: An update on pathogenesis and management

2015

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Hypercalcemia of malignancy is a common finding typically found in patients with advanced stage cancers. We aimed to provide an updated review on the etiology, pathogenesis, clinical presentation, and management of malignancy-related hypercalcemia. We searched PubMed/Medline, Scopus, Embase, and Web of Science for original articles, case reports, and case series articles focused on hypercalcemia of malignancy published from 1950 to December 2014. Hypercalcemia of malignancy usually presents with markedly elevated calcium levels and therefore, usually severely symptomatic. Several major mechanisms are responsible for the development of hypercalcemia of malignancy including parathyroid hormone-related peptide-mediated humoral hypercalcemia, osteolytic metastases-related hypercalcemia, 1,25 Vitamin D-mediated hypercalcemia, and parathyroid hormone-mediated hypercalcemia in patients with parathyroid carcinoma and extra parathyroid cancers. Diagnosis should include the history and physical examination as well as measurement of the above mediators of hypercalcemia. Management includes hydration, calcitonin, bisphosphonates, denosumab, and in certain patients, prednisone and cinacalcet. Patients with advanced underlying kidney disease and refractory severe hypercalcemia should be considered for hemodialysis. Hematology or oncology and palliative care specialists should be involved early to guide the options of cancer targeted therapies and help the patients and their closed ones with the discussion of comfort-oriented care.

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“…Hypercalcemia initially leads to impaired urinary concentration [26], then to reduced renal plasma flow and glomerular filtration rates, and finally results in multiple functional and structural derangements of the kidneys. Calcium deposition in renal tissue is also a factor stimulating renal damage [27]. In addition, mineral and bone disorders in CKD patients, along with the use of calcium-based phosphate binders, may result in vascular calcification and an associated increase in mortality due to cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 99%

A Comparison of the Long-Term Effects of Lanthanum Carbonate and Calcium Carbonate on the Course of Chronic Renal Failure in Rats with Adriamycin-Induced Nephropathy

et al. 2014

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Lanthanum carbonate (LA) is an effective phosphate binder. Previous study showed the phosphate-binding potency of LA was twice that of calcium carbonate (CA). No study in which LA and CA were given at an equivalent phosphate-binding potency to rats or humans with chronic renal failure for a long period has been reported to date. The objective of this study was to compare the phosphate level in serum and urine and suppression of renal deterioration during long-term LA and CA treatment when they were given at an equivalent phosphate-binding potency in rats with adriamycin (ADR)-induced nephropathy. Rats were divided into three groups: an untreated group (ADR group), a CA-treated (ADR-CA) group and a LA-treated (ADR-LA) group. The daily oral dose of LA was 1.0 g/kg/day and CA was 2.0 g/kg/day for 24 weeks. The serum phosphate was lower in the ADR-CA or ADR-LA group than in the ADR group and significantly lower in the ADR-CA group than in the ADR group at each point, but there were no significant differences between the ADR and ADR-LA groups. The serum phosphate was also lower in the ADR-CA group than in the ADR-LA group, and there was significant difference at week 8. The urinary phosphate was significantly lower in the ADR-CA group than in the ADR or ADR-LA group at each point. The urinary phosphate was also lower in the ADR-LA group than in the ADR group at each point, and significant difference at week 8. There were no significant differences in the serum creatinine or blood urea nitrogen among the three groups. In conclusion, this study indicated the phosphate-binding potency of LA isn’t twice as strong as CA, and neither LA nor CA suppressed the progression of chronic renal failure in the serum creatinine and blood urea nitrogen, compared to the untreated group.

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Reversible Renal Failure Caused by Hypercalcemia

Cited by 43 publications

References 25 publications

Hyperparathyroidism with hypercalcaemia in chronic kidney disease: primary or tertiary?

Hyperparathyroidism with hypercalcaemia in chronic kidney disease: primary or tertiary?

Hypercalcemia of malignancy: An update on pathogenesis and management

A Comparison of the Long-Term Effects of Lanthanum Carbonate and Calcium Carbonate on the Course of Chronic Renal Failure in Rats with Adriamycin-Induced Nephropathy

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