Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism

T. Kashitani, Hirofumi Makino, Y. Nagake, K. Hironaka, Kenichi Shikata, T. Ogura, Z. Ota

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.

Original languageEnglish
Pages (from-to)1189-1194
Number of pages6
JournalNippon Jinzo Gakkai shi
Volume35
Issue number10
Publication statusPublished - Oct 1993

Fingerprint

Primary Hyperparathyroidism
Hypercalcemia
Kidney
Necrosis
Nephrogenic Diabetes Insipidus
Biopsy
Polyuria
Parathyroid Neoplasms
Hyperparathyroidism
Bone Fractures
Sclerosis
Atrophy
Mitochondria
Epithelial Cells
Calcium
Carcinoma

ASJC Scopus subject areas

  • Nephrology

Cite this

Kashitani, T., Makino, H., Nagake, Y., Hironaka, K., Shikata, K., Ogura, T., & Ota, Z. (1993). Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Nippon Jinzo Gakkai shi, 35(10), 1189-1194.

Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. / Kashitani, T.; Makino, Hirofumi; Nagake, Y.; Hironaka, K.; Shikata, Kenichi; Ogura, T.; Ota, Z.

In: Nippon Jinzo Gakkai shi, Vol. 35, No. 10, 10.1993, p. 1189-1194.

Research output: Contribution to journalArticle

Kashitani, T, Makino, H, Nagake, Y, Hironaka, K, Shikata, K, Ogura, T & Ota, Z 1993, 'Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism', Nippon Jinzo Gakkai shi, vol. 35, no. 10, pp. 1189-1194.
Kashitani, T. ; Makino, Hirofumi ; Nagake, Y. ; Hironaka, K. ; Shikata, Kenichi ; Ogura, T. ; Ota, Z. / Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. In: Nippon Jinzo Gakkai shi. 1993 ; Vol. 35, No. 10. pp. 1189-1194.
@article{07a4cfa5c0194e218a111a7aa32f5b36,
title = "Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism",
abstract = "We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.",
author = "T. Kashitani and Hirofumi Makino and Y. Nagake and K. Hironaka and Kenichi Shikata and T. Ogura and Z. Ota",
year = "1993",
month = "10",
language = "English",
volume = "35",
pages = "1189--1194",
journal = "Japanese Journal of Nephrology",
issn = "0385-2385",
publisher = "Japanese Society of Nephrology",
number = "10",

}

TY - JOUR

T1 - Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism

AU - Kashitani, T.

AU - Makino, Hirofumi

AU - Nagake, Y.

AU - Hironaka, K.

AU - Shikata, Kenichi

AU - Ogura, T.

AU - Ota, Z.

PY - 1993/10

Y1 - 1993/10

N2 - We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.

AB - We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.

UR - http://www.scopus.com/inward/record.url?scp=0027672568&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027672568&partnerID=8YFLogxK

M3 - Article

C2 - 8264108

AN - SCOPUS:0027672568

VL - 35

SP - 1189

EP - 1194

JO - Japanese Journal of Nephrology

JF - Japanese Journal of Nephrology

SN - 0385-2385

IS - 10

ER -