Nephron 18: 321-325 (1977)
Hyperchloremia Associated with Membranoproliferative Glomerulonephritis W. H. Dreher1, S. W. Zimmerman and D. P. Simpson2 Nephrology Section, Department of Medicine, University of Wisconsin Center for Health Sciences, Madison, Wise.
Key Words. Hyperchloremia • Membranoproliferative glomerulonephritis
Introduction Hyperchloremia may exist in patients with nephrotic syndrome representing a compen sation for the decreased anionic plasma pro teins [8]. The only other reports of hyper chloremia associated with renal disease are in connection with hyperchloremic acidosis. Dis tal renal tubular acidosis (RTA) has been as sociated with interstitial renal disease such as 1 Supported by Training Grant AM05582 from the National Institute of Arthritis, Metabolism and Di gestive Diseases, the National Institutes of Health, Bcthesda, Md. (USA). 2 The authors would like to acknowledge the secre tarial assistance of Ms. Patricia Nash.
pyelonephritis and renal allograft rejection [2,9], and proximal RTA occurs during child hood with nephrotic syndrome accompanied by glycosuria and aminoaciduria [6,7], We have been aware of patients with the diagnosis of membranoproliferative glomer ulonephritis (MbPGN) who have elevated serum chlorides. A patient with this diagnosis who developed severe renal tubular acidosis prompted us to review serum chloride levels in this disorder. This report documents the presence of hyperchloremia in patients with MbPGN compared to other glomerulopathies associated with the nephrotic syndrome. At tempts have been made to define the etiology of the hyperchloremia.
Downloaded by: University of Leeds 129.11.21.2 - 1/15/2018 10:36:40 PM
Abstract. 16 patients with membranoproliferative glomerulonephritis had a mean serum chloride level significantly higher than that in normal subjects or in comparable groups of patients with nephrotic syndrome secondary to either systemic lupus erythematosus or to other primary nephrotic glomerular diseases. Differences in the severity of histologic alterations of the renal interstitium did not correlate with the different levels of serum chloride seen in these groups. The increased chloride concentration may be partially explained as a compensating reaction for a decrease in protein anions. However, a renal tubular acidifying defect demon strated in one of our patients may also contribute to the hyperchloremia in some cases.
Dreher/Zimmerman/Simpson
Methods 16 patients with MbPGN were compared with two other groups of patients with different types of renal disease: 12 patients with systemic lupus glomerulo nephritis (SLE) and 18 patients with nephrotic syn drome (NS) secondary to membranous, focal scleros ing, or minimal change glomerulonephropathy. The diagnosis of systemic lupus erythematosus was based on positive LE cell preparations and/or antinuclear antibodies plus a clinical course consistent with multi system involvement. The morphological basis for the diagnosis of all the above mentioned renal diseases and procedures for processing renal biopsies and staining techniques have been previously described [I], Laboratory determinations were made by the fol lowing methods: C3 by radial immunodiffusion, elec trolytes, serum albumin, total protein, and creatinine by sequential multiple analyzer. Serum parathormone levels were performed by Mayo Medical Laboratories, Rochester, Minn. Four patients with MbPGN were studied following a short ammonium chloride loading test as described by Wrong and Davies [9]. All patients were given liquid NH4CI at a dose of 0.1 g/kg. Urine was collected under mineral oil, and urine pH was determined using a Radiometer pH meter. Statistical analysis of the data was determined using Student’s t test, and calculations of the linear cor relations for table II were performed with chloride as the dependent variable. Biopsies were evaluated for the extent of interstitial and tubular disease. Two reviewers, without prior knowledge of the diagnosis, graded biopsies. A grading system of 0 to 4 + was used for extent of interstitial edema, fibrosis, or cellular infiltrate and tubular casts, swelling, or degeneration.
Results 12 out of 16 patients with MbPGN had serum chloride values greater than 105 mEq/1. Normal for this laboratory is 95-105 mEq/1. A random screening of 135 patients with rou tine electrolyte determinations revealed a mean serum chloride of 99 mEq/1. The mean serum chloride value for the 16 patients was 108.2 mEq/1 which was significantly higher
(p
Hyperchloremia Associated with Membranoproliferative Glomerulonephritis W. H. Dreher1, S. W. Zimmerman and D. P. Simpson2 Nephrology Section, Department of Medicine, University of Wisconsin Center for Health Sciences, Madison, Wise.
Key Words. Hyperchloremia • Membranoproliferative glomerulonephritis
Introduction Hyperchloremia may exist in patients with nephrotic syndrome representing a compen sation for the decreased anionic plasma pro teins [8]. The only other reports of hyper chloremia associated with renal disease are in connection with hyperchloremic acidosis. Dis tal renal tubular acidosis (RTA) has been as sociated with interstitial renal disease such as 1 Supported by Training Grant AM05582 from the National Institute of Arthritis, Metabolism and Di gestive Diseases, the National Institutes of Health, Bcthesda, Md. (USA). 2 The authors would like to acknowledge the secre tarial assistance of Ms. Patricia Nash.
pyelonephritis and renal allograft rejection [2,9], and proximal RTA occurs during child hood with nephrotic syndrome accompanied by glycosuria and aminoaciduria [6,7], We have been aware of patients with the diagnosis of membranoproliferative glomer ulonephritis (MbPGN) who have elevated serum chlorides. A patient with this diagnosis who developed severe renal tubular acidosis prompted us to review serum chloride levels in this disorder. This report documents the presence of hyperchloremia in patients with MbPGN compared to other glomerulopathies associated with the nephrotic syndrome. At tempts have been made to define the etiology of the hyperchloremia.
Downloaded by: University of Leeds 129.11.21.2 - 1/15/2018 10:36:40 PM
Abstract. 16 patients with membranoproliferative glomerulonephritis had a mean serum chloride level significantly higher than that in normal subjects or in comparable groups of patients with nephrotic syndrome secondary to either systemic lupus erythematosus or to other primary nephrotic glomerular diseases. Differences in the severity of histologic alterations of the renal interstitium did not correlate with the different levels of serum chloride seen in these groups. The increased chloride concentration may be partially explained as a compensating reaction for a decrease in protein anions. However, a renal tubular acidifying defect demon strated in one of our patients may also contribute to the hyperchloremia in some cases.
Dreher/Zimmerman/Simpson
Methods 16 patients with MbPGN were compared with two other groups of patients with different types of renal disease: 12 patients with systemic lupus glomerulo nephritis (SLE) and 18 patients with nephrotic syn drome (NS) secondary to membranous, focal scleros ing, or minimal change glomerulonephropathy. The diagnosis of systemic lupus erythematosus was based on positive LE cell preparations and/or antinuclear antibodies plus a clinical course consistent with multi system involvement. The morphological basis for the diagnosis of all the above mentioned renal diseases and procedures for processing renal biopsies and staining techniques have been previously described [I], Laboratory determinations were made by the fol lowing methods: C3 by radial immunodiffusion, elec trolytes, serum albumin, total protein, and creatinine by sequential multiple analyzer. Serum parathormone levels were performed by Mayo Medical Laboratories, Rochester, Minn. Four patients with MbPGN were studied following a short ammonium chloride loading test as described by Wrong and Davies [9]. All patients were given liquid NH4CI at a dose of 0.1 g/kg. Urine was collected under mineral oil, and urine pH was determined using a Radiometer pH meter. Statistical analysis of the data was determined using Student’s t test, and calculations of the linear cor relations for table II were performed with chloride as the dependent variable. Biopsies were evaluated for the extent of interstitial and tubular disease. Two reviewers, without prior knowledge of the diagnosis, graded biopsies. A grading system of 0 to 4 + was used for extent of interstitial edema, fibrosis, or cellular infiltrate and tubular casts, swelling, or degeneration.
Results 12 out of 16 patients with MbPGN had serum chloride values greater than 105 mEq/1. Normal for this laboratory is 95-105 mEq/1. A random screening of 135 patients with rou tine electrolyte determinations revealed a mean serum chloride of 99 mEq/1. The mean serum chloride value for the 16 patients was 108.2 mEq/1 which was significantly higher
(p
