The pathohistological entity, membranoproliferative glomerulonephritis, is serologically associated with decreased components of complement. However, patients with hypogammaglobulinemia are rare. A patient with these features is reported here.

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In 42 renal biopsy specimens from 40 systemic lupus erythematosus (SLE) patients, the glomerular histology and immunofluorescence findings, according to the grades and patterns of IgG deposits, were compared with data for clinical and serological tests including the circulating immune complexes (CIC) and anti-dsDNA antibodies. The levels of CIC measured by solid phase C1q binding assay (SPC1q-IC) were highest in the group showing mesangial and segmental capillary wall IgG deposits, with clinically active symptoms, whereas the CIC by conglutinin binding assay (SPKg-IC) revealed poor correlations. The serum levels of anti-dsDNA antibodies were significantly correlated histologically with both mesangial cell proliferation and karyo rrhexis and/or pycnosis, and by immunofluorescence with the grades of mesangial IgG deposits. These findings suggest that anti-dsDNA antibodies may contribute to the mesangial lesions of lupus nephritis and that SPC1q-IC is related to active renal disease which shows diffuse mesangial and segmental capillary wall IgG deposits.

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A study was undertaken to determine whether or not the glomerular permeability per se becomes a determinant of the localization of immune complex (IC) in active chronic serum sickness. ICR mice were made nephrotic by single injections of daunomycin (DM), At 2 weeks after the DM injection, both normal and DM-nephrotic mice were immunized by giving intraperitoneal injections of horse spleen apoferritin (HAF) on alternate days. At 14 and 28 days after the initiation of immunization, in animals without DM treatment, IgG, C3 and HAF were found in the mesangial areas but not in the capillary wall. Few abnormalities were observed by light microscopy, but mesangial dense deposits were detected by electron microscopy in the glomeruli of these animals. In contrast, DM-treated animals revealed marked capillary wall deposits of immunoreactants with an equal amount of mesangial deposits. Examinations by light microscopy demonstrated proliferative glomerular lesions, while those by electron microscopy showed dense deposits in the subepithelial, subendothelial and mesangial areas. The findings were more conspicuous in animals sacrificed at 28 days after immunization. Between DM-treated and non-treated animals, no significant difference was detected in terms of the plasma anti-HAF antibody level, antibody avidity and disappearance rate of HAF from the circulation. The significant shift of immune deposits from the mesangium to the capillary walls detected in DM mice is therefore considered to have resulted from an increased permeability of the glomerular basement membrane (GBM) per se induced by the administration of DM.

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The urinary Tamm Horsfall glycoprotein (T-HGP) excretion was measured by electroimmunoassay in 34 healthy subjects with normal renal function (20 males and 14 females). The relationships between the urinary T-HGP and other urinary indicators were also investigated. The urinary T-HGP concentration was 47.6±18.3 mg/l (mean±S.D.) for males and 37.3±23.6 mg/l for females, indicating no significant difference between the sexes. The T-HGP/urinary creatinine (mg⋅T-HGP/g⋅creatinine) ratio was 30.2±9.1 for males and 67.6±26.8 for females. It was thus significantly greater in the latter (P<0.001). Highly significant correlations were found between the T-HGP value and the following four indicators: urinary creatinine (Cr) (r=0.593, P<0.001), urinary osmotic pressure (u-Osm) (r=0.704, P<0.001), urinary protein concentration (r=0.740, P<0.001) and sodium concentration (r=0.492, P<0.01). There was no significant correlation between the urinary T-HGP and potassium. A sex difference in the regression equations was noted only in the case of the relationship between T-HGP and creatinine, as follows: T-HGP (mg/1) 10.4 + 22.4×Cr (g/l) for males and T-HGP=0.9+68.7×Cr for females. The regression coefficients were significantly different between the sexes (P<0.025). The urinary β₂-microglobulin (β₂-M), α ₁-microglobulin (α₁-M) and N-acetyl-β-D-glucosaminidase (NAG) activity were measured in 19 subjects. T-HGP was not related with these tubular proteins. The above results suggest that the urinary T-HGP concentration in normal subjects reflects the urine osmolarity and is independent of other tubular proteins which derive from the proximal tubules.

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The urinary Tamm Horsfall glycoprotein (T-HGP) excretion was estimated by the electroim-munoassay method in 79 patients with various renal diseases and was compared with that in normal subjects. In the patient group, the urinary T-HGP concentration was 12.9±12.5 mg/l (mean±S.D.) and the daily T-HGP excretion was 16.9±14.1 mg/day, respectively. Good correlations were found between the urinary T-HGP concentration and the urine osmolarity (r=0.696, P<0.001), sodium (r=0.509, P<0.001) and creatinine (r= 0.343, P<0.01). A significant correlation between the daily T-HGP excretion and creatinine clearance (Ccr) was also noted (r=0.650, P<0.001). These results suggest that the urinary T-HGP concentration reflects the urine osmolarity and urinary solute excretion. Furthermore, the daily T-HGP excretion may reflect the functioning nephron mass. The urinary T-HGP excretion was influenced by the glomerular filtration rate. The T-HGP concentration was 19.2±13.8 mg/l and the daily T-HGP excretion was 24.3±14.5 mg/day in subjects with a Ccr greater than 70 ml/min, while the corresponding values were 5.9±13.9 mg/l and 6.1±8.5 mg/day, respectively, in subjects with a Ccr less than 30 ml/min. The values in the former group were significantly higher. On the other hand, T-HGP/Ccr (μg/ml) was significantly higher in the renal failure patients (Ccr less than 30 ml/min). There was no significant difference in T-HGP excretion between patients with primary glomerular diseases and those with renal involvement associated with systemic diseases. The urinary T-HGP concentration and the daily T-HGP excretion were 15.5±12.0 mg/l and 21.9±13.4 mg/day in the patients with primary glomerular diseases, while the corresponding values were 17.3±8.8 mg/l and 24.7±16.7 mg/day, respectively, in the patients with systemic diseases. Eighteen patients with normal renal function (Ccr greater than 70 ml/min) were compared with age and Ccr-matched control subjects. The urinary T-HGP concentration and the daily T-HGP excretion of the patient group were significantly lower than those of the control group. These results suggest that the urinary T-HGP excretion decreases in patients with renal diseases in spite of a well-preserved renal function.

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The bioactivity of parathyroid hormone (PTH) was measured by guanyl nucleotide amplified adenylate cyclase assay. Of 73 uremic patients on maintenance hemodialysis for over 4 years, 49 (67%) had PTH activities exceeding 100 pg/ml equivalent to human PTH (1-34). All patients had elevated c-terminal immunoreactive PTH (c-iPTH) and mid-region specific immunoreactive PTH (m-iPTH). The correlation between the PTH activity and iPTH was significant, but some patients had mildly elevated values of iPTH and considerably high PTH activity. Many of the patients with elevated PTH activity suffered from bone or joint pain. It is suggested that some patients had more developed bone disease than would be expected from the values of iPTH. Although the sensitivity of the present modified adenylate cyclase assay is at present insufficient to detect mild hyperparathyroidism, the technique may be useful for the management of secondary hyperparathyroidsm due to chronic renal failure.

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A rare case of diabetic glomerulosclerosis with nephrotic syndrome in early pregnancy is reported. The patient was a 27-year-old woman who had been diagnosed as having diabetes mellitus 10 years previously. She developed nephrotic syndrome with severe hypertension in the 10th week of gestation. Renal biopsy performed three months after artificial abortion, revealed diabetic glomeru-losclerosis with mesangiolysis. Her renal function deteriorated progressively. The hemodynamic alterations in early pregnancy and severe hypertension could be closely related to the onset of nephrotic syndrome.

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The effect of the converting enzyme inhibitor, enalapril, on systolic blood pressure (SBP) and plasma renin substrate (PRS) was studied in sodium loaded and non-sodium loaded spontaneously hypertensive rats (SHR). (1) Before enalapril administration, SBP and PRS of the SHR gradually increased with age and this increase was greater in sodium loaded SHR than in non-sodium loaded SHR, in spite of a decreased plasma renin activity (PRA) in the former. (2) During administration of enalapril, SBP decreased in parallel with a decline of PRS in non-sodium loaded SHR and with a plateau of PRS in sodium loaded SHR. (3) After cessation of enalapril, SBP increased markedly in parallel with PRS in both groups in spite of a decreased PRA. (4) Over the whole course of age, there was a positive correlation between SBP and PRS, regardless of whether enalapril was administered or not. (5) These results suggest that PRS may play an important role in the genesis of hypertension in SHR.

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Urinary kallikrein was measured in patients with mesangial proliferative glomerulonephritis. No patients had hypertension, nephrotic syndrome or severe renal dysfunction. Quantitative analysis of the histological changes and establishment of indices of glomerular lesions (IGL) and tubular atrophy (T/S) in renal biopsy specimens were carried out. In 24 patients, the kallikrein excretion was found to be positively correlated with the creatinine clearance (p <0.05), negatively correlated with IGL (p <0.01) and positively so with the mean value of T/S (p <0.01). In spot urine tests on 30 patients, the kallikrein activity was positively correlated with the creatinine clearance (p <0.001) and Fishberg's maximum (p <0.02), negatively correlated with IGL (p <0.01) and positively so with the mean value of T/S (p <0.01). Kallikrein excretion in the 24-hour urine showed a significantly positive correlation with that detected in the spot urine tests (r = 0.878, p <0.001). These results indicate that the urinary kallikrein may reflect the renal interstitial injury and that its application may be of clinical use in the diagnosis of renal diseases.

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A case of chronic thyroiditis complicated by nephrotic syndrome and marked hydroureterone-phrosis in a 38-year-old female is reported. Renal biopsy yielded findings closely resembling mem-branoproliferative glomerulonephritis. Localized thyroglobulin was identified in the glomerular base-ment membrane by the indirect immunoperoxidase method. Contracted bladder due to intersitial cystitis was thought to be the main cause of the hydroureteronephrosis. Thyroid related immune complex was regarded as the main factor in the developing nephropathy and contracted bladder in this case. Various antigens such as DNA, hemolytic streptococcus, staphylococcus, tumor antigen and type B hepatitis virus have been indicated as antigens for some cases of immune complex type nephritis. [1] -[5] Recently, some rare cases of immune complex type nephritis with components of the thyroid gland as the antigen have been reported. [6]-[14] The authors report here a case of chronic thyroiditis complicated by nephrotic syndrome and contracted bladder showing obvious hydroureteronephrosis with confirmed evidence of thyroglobulin deposits within the glomeruli.

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Three kinds of kidney calculi in the powdered and the massive state were subjected to dissolution in an aqueous suspension containing H-R. MAP and CaP calculi were readily dissolved in the suspension irrespective of their morphology, and it is expected that the technique can be applied for the removal of kidney calculi in clinical experiments. The method was useful in the case of powdered CaOx but was not so effective for the massive state.

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We report a case of a 6-year-old girl with an atypical form of Type 2 membranoproliferative glomerulonephritis (MPGN). She was admitted with gross hematuria and proteinuria, which were found to decrease gradually on no specific treatment. Serological studies disclosed persistent hypocomple-mentemia. A renal biopsy was performed, two years after onset of the disease, because of persistent hypocomplementemia and reappearance of microhematuria. Examination by light microscopy demon-strated only minor glomerular abnormalities, with double contours in a few capillaries and some deposits in Bowman's capsule. However, electron microscopy revealed intramembranous dense deposits typical of Type 2 MPGN, and immunofluorescence showed deposition of C₃ in the mesangium, and along segments of the capillary walls and Bowman's capsule. A diagnosis of atypical Type 2 MPGN was made, and alternate-day prednisolone therapy was started. The serum level of C₃ subsequently increased, only to decrease again when prednisolone was discontinued. A repeat biopsy revealed findings similar to the first, except for a decline in the intensity of C₃ by immunofluorescence microscopy. On the basis of these observations, we consider that this patient represented a mild form, or an early stage of typical Type 2 MPGN.

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A patient with hypocomplementemic mesangiocapillary glomerulonephritis had two different coexistent serum factors, which may be able to activate the alternative complement pathway: One was immunologically identical with C3 nephritic factor and the other was a non-IgG factor. In this case, the changes in the complement system indicated that the level of C5 was extremely reduced at the time when the two factors appeared, while the CS levels were almost normal only when C3 nephritic factor appeared.

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SHR demonstrated exaggerated natriuresis following acute saline infusion. This was accompanied by decreased activity of the efferent renal sympathetic nerve. However, such exaggerated natriuresis was no longer observed in SHR after bilateral vagotomy.

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