Medullary Sponge Kidney Associated with Parathyroid Adenoma

Stella, Francesco; Massry, Shaul G.

doi:10.1159/000180204

Cited by 16 publications

(4 citation statements)

References 8 publications

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“…The stones passed with MSK are typically composed of calcium oxalate with or without phosphate and apatite [4,9], A variety of renal functional and metabolic distur bances contribute to stone formation in MSK, including abnormalities in urinary acidification [6,7,9] and/or calcium excretion [4,7,13]. As the spectrum of meta bolic abnormalities is little different from that observed in the general population of stone formers [3,9,14], patients with MSK should have an incidence of staghorn disease similar to that observed in the general stone forming population.…”

Section: Discussionmentioning

confidence: 99%

Medullary Sponge Kidney and Staghorn Calculi

Nunley

Sica²,

Smith³

1990

Urol Int

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We describe a 65-year-old female with bilateral staghorn calculi who presented with a Proteus mirabilis perinephric abscess secondary to a ruptured lower pole hydrocalyx. Radiologic evidence was consistent with underlying medullary sponge kidney (MSK) disease. Despite expectations to the contrary, MSK, a disease notable for many risk factors capable of precipitating staghorn disease, is rarely associated with coexistent staghorn calculi. A discussion of the concurrent risk factors and a possible hypothesis regarding the lack of coexistence follows.

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Section: Discussionmentioning

confidence: 99%

Medullary Sponge Kidney and Staghorn Calculi

Nunley

Sica²,

Smith³

1990

Urol Int

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“…This theory, though attractive, does not explain why only a few patients with primary hyperparathyroidism experience MSK nor why renal calcification is not a universal feature of this disease [3]. However, in many patients with this association pri mary hyperparathyroidism was the main cause of hypercalciuria and recurrent stone formation: in fact, after the removal of the adenoma urinary excretion of calcium became normal and there was no recurrence of new stones [8,10,11]. This was also observed in 3 of our patients with parathyroid adenoma, followed for 3-6 years after surgery.…”

Section: Discussionmentioning

confidence: 99%

Medullary Sponge Kidney and Hyperparathyroidism -a Puzzling Association

Maschio

Tessitore

D’Angelo³

et al. 1982

Am J Nephrol

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28 adult patients with radiological evidence of medullary sponge kidney (MSK) were studied. Hypercal-cemia and increased serum parathyroid hormone (PTH) values were found in 10 patients (36%). In 7 of them, parathyroid surgery was performed: a single adenoma was found in 6 cases and multiple-gland hyperplasia in 1 case. After surgery, 3 patients had normalization of calcium metabolism; 4 patients had persistence of hypercalciuria with progressive increase in serum PTH values (and recurrence of the adenoma in 1 case). Of the remaining patients, 10 (36%) had definite or marginal hypercalciuria, resulting from renal calcium leak in 8 and from intestinal calcium hyperabsorption in 2 of them. In 8 patients (28%), no evidence of disordered calcium metabolism was found. The association of MSK and hyperparathyroidism is not a chance occurrence. MSK might be a renal anatomical complication of primary hyperparathyroidism, or it might be regarded as an anatomic substrate – or rather as a consequence -of prolonged hypercalciuria, regardless of its pathogenesis. The lack of disordered calcium metabolism in a considerable number of patients, however, shows that the enigma of MSK is still far from being solved.

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“…PTH causes the release of bone mineral (60). It stimulates the renal call1-a-25 (OH)D3 hydroxylase to increase the production of l-a-25 (OH)2D3 (1,25 D3)' which increases calcium absorption by the small intestine (58) and colon (59). It reduces renal tubule phosphorus reabsorption, causing hypophosphatemia, which may also stimulate 1,25 D3 production, and increases renal tubule calcium reabsorption (61 causes hypercalciuria, just as a high meat intake can cause hyperuricosuria; the increased tubule calcium reabsorption, however, permits the kidney to increase calcium excretion only at the expense of an increased filtered load of calcium.…”

Section: Pathogenesis Of Stonesmentioning

confidence: 99%