Biomedical subjects

A B Magil

Publications and source records attributed to A B Magil.

At least 37 records · Page 2Linked to original sources

PubMed1989

Monocytes and focal glomerulosclerosis.

It has been suggested that focal glomerulosclerosis (FGS) is analogous to atherosclerosis. Because monocytes and their derivatives are involved in the latter, these cells may be involved in the development of the former. To investigate this possibility a combined histochemical and ultrastructural study of FGS was done. Sections from 13 biopsies showing FGS were stained for either nonspecific esterase or lysozyme to detect monocytes and their derivatives. These include foam cells (lipid-containing macrophages) in which there was positive cytoplasmic staining for both nonspecific esterase and lysozyme. Twenty-one of 29 glomeruli (72%) with segmental sclerotic lesions contained monocytes and/or foam cells, whereas only 18 of 251 glomeruli (7%) without the lesions demonstrated these cells (p less than 0.0001). The mean number of monocytes and/or foam cells in segmentally sclerotic glomeruli was 2.0 +/- 1.7 compared with 0.2 +/- 0.3 for uninvolved glomeruli (p less than 0.01). In glomeruli with sclerotic lesions foam cells predominated over monocytes. Neutral lipid was observed focally and segmentally in 29 of 35 biopsies with FGS. Electron microscopy in 23 biopsies consistently demonstrated intracapillary cells with monocytic features but few foam cells in very early lesions characterized by epithelial cell changes but no or minor glomerular tuft alterations. With progression, the relative number of monocytes declined but foam cells were observed more frequently. These results suggest that monocytes and their derivatives are involved in the development of FGS.

Carboxylesterase↗

PubMed1988

Prognostic factors in diffuse proliferative lupus glomerulonephritis.

A number of clinical laboratory and biopsy-derived parameters were assessed for their prognostic significance in the short (24 months), intermediate (60 months) and long terms in 45 patients (43 female, 2 male) with diffuse proliferative lupus glomerulonephritis (DPGN). The factors evaluated were serum creatinine (SCr) and urinary protein at time of biopsy, initial dose of prednisone and immunosuppressive after biopsy, activity index (AI), chronicity index (CI), their individual components, extent of extraglomerular (tubulo-interstitial) immune deposits (EGD) and mean number of intraglomerular monocytes per glomerulus (NSE index). Using proportional hazards analysis to evaluate the parameters, SCr (P = 0.003), AI (P = 0.005) and NSE index (P = 0.038) were shown to be significant predictors of outcome when all variables except the components of AI and CI were considered. When AI and CI were omitted but their components included, SCr (P = 0.0005), NSE index (P = 0.024), extent of karyorrhexis (P = 0.035) and glomerulosclerosis (P = 0.033) were then demonstrated to be significant prognostic factors of DPGN. The results suggest that intraglomerular monocyte infiltration has a protective effect and confirm that AI index is a relatively powerful predictor of outcome. Histologic and nonhistologic biopsy factors contribute significant additional prognostic information to that provided by SCr.

Adult↗

PubMed1988

Glomerular disease in hypercholesterolemic guinea pigs: a pathogenetic study.

Recent evidence suggests a role for lipid deposition in the pathogenesis of some forms of glomerular disease. To gain further insight into this phenomenon guinea pigs (GP) were fed a 2% cholesterol (HC) diet and compared to GP on a normal diet (C). Serial observations were made 5, 10, 30 and 70 days after the initiation of the experiment. HC gained less weight than C (P less than 0.001) and developed hemolytic anemia after 30 days. At all time periods serum total cholesterol (TC) was significantly elevated in HC (P less than 0.001). High density lipoprotein-cholesterol and total phospholipids (PL) were significantly higher in HC at days 30 and 70. Lipoprotein-X was detected in HC serum. The relative proportion (%) of cholesteryl ester (CE) at day 70 was significantly higher in HC than in C when renal cortical lipids were analyzed (P less than 0.017). Renal function was normal in both groups throughout the 70 days. The HC group developed proteinuria and hematuria (proteinuria, HC = 22.1 +/- 7.2 mg/24 hr; C, 6.4 +/- 2.3 mg/24 hr), which was detected at day 70 but not at day 30. HC developed significant progressive mesangial expansion which was first evident at day 30. In HC only oil red 0 material was first detected in glomeruli at day 5 and was very conspicuous at day 70. Increased intraglomerular monocyte numbers were detected at day 70 (P less than 0.017) but not at day 30 in HC. No glomerulosclerosis was observed in GP's with drug-induced hemolysis on a normal diet. To see the effect of high protein intake on HC GP's, a group of GP's was put on a HC diet for 30 days followed by a 2% cholesterol-high protein (HCHP) diet for 40 days. Compared to HC GP's, the HCHP group showed significantly higher serum TC and PL (P less than 0.017), mesangial expansion (P less than 0.01) and proteinuria (P less than 0.01). The results indicate that hypercholesterolemia plays an important role in the pathogenesis of glomerulosclerosis in this model and that the process appears to be mediated, at least in part in the later stages, by monocytes. The addition of protein to the HC diet augments these effects.

Animals↗

PubMed1988

Sodium thiosulfate prevents cisplatin-induced hypomagnesemia.

Clearance studies were performed in four groups of male Wistar rats to assess the protective effect of sodium thiosulfate on cisplatin-induced hypomagnesemia. In group I, sodium thiosulfate (400 mg/kg) was injected intraperitoneally once weekly for 3 consecutive weeks. In group II, only cisplatin (2.5 mg/kg) was administered. In group III, both cisplatin (2.5 mg/kg) and sodium thiosulfate (400 mg/kg) were injected via the intraperitoneal route. When both drugs were administered together, they were injected into different parts of the peritoneal cavity. In group IV cisplatin was administered intraperitoneally and sodium thiosulfate intravenously. Sodium thiosulfate prevented a rise in plasma creatinine. The overall glomerular filtration rates of groups III and IV were the same as in group I. Hypomagnesemia was noted in group II, whereas in groups I, III, and IV the plasma magnesium level remained unchanged. The fractional excretion of magnesium was also higher in group II than in groups I, III, and IV. These differences persisted for the duration of the study. These results suggest that concurrent injections of sodium thiosulfate intraperitoneally or intravenously prevented the hypomagnesemic and the nephrotoxic effects of cisplatin and can be of clinical significance.

Animals↗

PubMed1987

IgA nephropathy. Evaluation of prognostic factors in patients with moderate disease.

Previous studies of IgA nephropathy have demonstrated a number of prognostically significant clinical and pathological factors in groups of patients with the full histological spectrum of the disease. Whether these factors can be applied to a group of IgA nephropathy patients with disease of moderate degree is unknown. Forty patients (9 females, 31 males) with grade III IgA nephropathy (no more than 10% obsolete glomeruli and little or no interstitial fibrosis) were evaluated with respect to age, sex, degree of proteinuria, history of recurrent gross hematuria, hypertension, extent and type of segmental glomerulosclerosis, demonstration of IgG and/or IgM in deposits, presence of peripheral capillary deposits, whether or not there were crescents, and extent of vascular sclerosis. The mean age was 29.6 +/- (SD) 13.1 years. Sixteen patients presented with recurrent gross hematuria, and 24 had microscopic hematuria and proteinuria as the initial manifestation. Hypertension was seen in 5 patients. The mean serum creatinine concentration was 1.09 +/- 0.47 mg/dl (96.4 +/- 41.5 mumol/l), and the mean 24-hour urinary protein was 1.5 +/- 1.3 g. Nine patients had proteinuria greater than or equal to 2.0 g/24 h. Thirty-two patients demonstrated segmental glomerulosclerosis in their biopsies, 13 of which had more than 10% of the glomeruli involved. Seven patients developed established renal failure (Cr greater than or equal to 2.0 mg/dl; 176.8 mumol/l). The 60-and 100-month renal survival rates were 96 and 52%. Life table analysis disclosed that only the degree of proteinuria (greater than or equal to 2.0 g/24 h; p less than 0.05) and the extent of segmental glomerulosclerosis (p less than 0.025) were of prognostic significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1987

The distinction between acute renal transplant rejection and cyclosporine nephrotoxicity: value of duplex sonography.

Although sonography is useful in the evaluation of renal transplants, there are no objective sonographic findings for reliably differentiating acute rejection from cyclosporine nephrotoxicity. This study was undertaken to determine the role of pulsed Doppler flow analysis (duplex sonography) in making this distinction. Duplex Doppler sonography was performed in 106 patients with normally functioning transplanted kidneys and in 34 patients with renal transplant dysfunction who underwent percutaneous biopsy. Renal vascular impedance was estimated in the segmental, interlobar, and arcuate arteries by calculating the ratio of end-diastolic minimum velocity to systolic peak velocity (diastolic/systolic ratio). In the healthy control subject, the diastolic/systolic velocity ratios varied in the different arterial segments, ranging from a mean of 0.23 in the segmental arteries to a mean of 0.32 in the arcuate arteries. Seventeen patients experienced acute rejection: eight of the nine with acute vascular rejection had abnormal Doppler ratios; eight patients with acute cellular rejection had normal ratios. Nine patients with cyclosporine nephrotoxicity all had normal duplex scans. Seven patients with chronic rejection had normal ratios. One patient with hemolytic-uremic syndrome had an abnormal flow pattern. These findings indicate that duplex sonography may be useful in differentiating acute vascular rejection from cyclosporine nephrotoxicity in the transplanted kidney.

Adult↗

PubMed1986

Lupus glomerulonephritis with thrombotic microangiopathy.

Well-documented cases of systemic lupus erythematosus (SLE) with thrombotic microangiopathy (TMA) are rare. Renal biopsy in a 25-year-old woman with SLE who was in renal failure demonstrated proliferative lupus glomerulonephritis with arteriolar thrombosis and the arterial intimal changes of TMA. No staining of vessels for immunoglobulins or complement was found by direct immunofluorescence. Fibrillar and flocculent deposits were seen in the widened and rarefied subendothelial space in a small artery and two glomeruli, one of which also contained electron-dense deposits. The vascular findings, which are those of TMA, are distinct from the immune complex vasculopathy of SLE.

Adult↗

PubMed1986

Long-term morphological and biochemical observations in cisplatin-induced hypomagnesemia in rats.

A model of cisplatin (cis-diamminedichloroplatinum II) induced hypomagnesemia with renal magnesium wasting was developed in rats. Following three weekly intraperitoneal injections of cisplatin (2.5 mg/kg body weight) hypomagnesemia was evident after the second injection of cisplatin and persisted for at least 24 weeks after the last injection. The plasma magnesium concentration was 0.69 +/- 0.01 mM in cisplatin-treated rats and 0.79 +/- 0.01 mM in control rats 24 h after the second injection (less than 0.01). Despite a lower plasma magnesium concentration in cisplatin-treated rats, the fractional urinary excretion of magnesium was similar in both groups, indicating inappropriate renal magnesium excretion in cisplatin-treated rats. Rat kidneys fixed in situ by arterial infusion were examined by light and electron microscopy at the following times: 24 h after the first and second injections and 48 h and 1, 4, 8, 16, and 24 weeks after the third injection. Focal necrosis of the proximal tubule cells in the outer stripe of the medulla (S3 segment) was noted 24 h after the second injection. Following this, there was dilatation of the S3 segment proximal tubules which were lined by variably flattened epithelial cells devoid of brush borders. Many of these cells had enlarged, hyperchromatic nuclei, and few mitoses were observed. These changes were most extensive at 4 weeks, diminished after this, but were still present focally at 24 weeks. In this model the cisplatin-induced hypomagnesemia persists long after discontinuation of therapy as in humans, and the S3 segment is the prime target of the cisplatin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Studies on the pathogenesis of cisplatin-induced hypomagnesemia in rats.

After three weekly intraperitoneal injections of cisplatin (2.5 mg/kg body wt), male Wistar rats developed chronic hypomagnesemia, which was evident from the second week and persisted throughout the 8-week experiments. Plasma magnesium concentration was 0.69 +/- 0.01 mM in cisplatin-treated rats compared to 0.80 +/- 0.02 mM in pair-fed control rats (P less than 0.01) in the eighth week of experimentation. Despite a similar dietary magnesium intake, urinary excretion of magnesium in cisplatin-treated rats was inappropriately high, relative to the lower plasma magnesium concentration, indicating the presence of renal magnesium wasting induced by cisplatin. During the 3 weeks of cisplatin injections, metabolic balance studies indicated abnormal renal excretion and a reduction in the fractional intestinal absorption of magnesium. A compensatory period of significantly greater retention of magnesium then occurred in cisplatin-treated rats beginning in the fourth week. Clearance and recollection micropuncture studies in a separate group of rats revealed normal magnesium and calcium transport in the superficial proximal and distal nephron. Following acute MgCl2 infusion, the urinary excretion of magnesium and calcium were significantly higher in cisplatin-treated rats than in control rats; however, micropuncture studies of superficial nephrons failed to demonstrate abnormal transport of these divalent cations. It is possible, therefore, that 7 weeks of cisplatin treatment led to tubular adaptation that might have obscured the defect in magnesium reabsorption. Morphological examination indicated that pathological changes were confined to the S3 segment of proximal corticomedullary nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Histogenesis of glomerular crescents. Immunohistochemical demonstration of cytokeratin in crescent cells.

Recent studies have suggested that crescents are primarily of monocytic origin and that epithelial cells are a minor factor in their composition. Frozen sections of renal biopsies from 11 cases of crescentic glomerulonephritis (CGN) and 5 controls (2 acute interstitial nephritis, 1 focal glomerulosclerosis, 1 benign recurrent hematuria, 1 normal kidney) were stained for intracellular cytokeratin (CK) with a mouse monoclonal anti-CK antiserum (PKK1) and nonspecific esterase (NSE) activity. Indirect immunofluorescence with PKK1 antiserum showed that in all biopsies there was positive staining of collecting duct and proximal and distal tubular epithelium but no reactions in blood vessels or interstitium. In control case glomeruli there was no staining of the tuft, including the visceral epithelium. In all cases some parietal epithelium was CK-positive. In 4 CGN biopsies the majority of the crescents showed cytoplasmic staining for CK in more than 50% of the crescent cells. In 2 cases most crescents contained between 10-50% CK-positive cells, whereas in 5 biopsies little or no CK was present in the majority of crescents. In all but one CGN case the majority of crescents contained fewer than 30% NSE-positive cells (monocytes). Electron microscopy demonstrated intermediate filaments in many crescent cells and scattered desmosomes within crescents. The results indicate that epithelial cells, probably of parietal epithelial origin, contribute significantly to crescent formation.

Antibodies, Monoclonal↗

PubMed1984

Tubulo-interstitial disease in lupus nephritis. A morphometric study.

To test the hypothesis that immune complex deposition can mediate tubulo-interstitial damage in lupus nephritis, a correlative immunofluorescent (IF) and morphometric study of 43 renal biopsies from 39 patients with diffuse proliferative lupus glomerulonephritis was done. The point-counting method was used to determine the percentage of the cortical tubulo-interstitial system occupied by the mononuclear cell infiltrates (infiltrate index) and by the interstititum (interstitial index). The estimated amount of deposits containing immunoglobulin along tubular basement membranes and within the interstitium was expressed as a percentage of tubulo-interstitial volume. Interstitial cell infiltrates were present in 40 of the 43 biopsies and tubulo-interstitial immune deposits were noted in 29 biopsies. Linear regression analysis showed a statistically significant correlation between interstitial and infiltrate indices (r = 0.553, P less than 0.001). Correlations between (a) the extent of immune deposits and interstitial index (r = 0.239) and (b) immune deposits and infiltrate index (r = 0.280) were not significant. The results do not support the hypothesis that immune deposits mediate tubulo-interstitial injury and suggest that the damage is effected by the inflammatory cell infiltrates.

Adolescent↗

PubMed1984

Diffuse proliferative lupus glomerulonephritis. Determination of prognostic significance of clinical, laboratory and pathologic factors.

Clinical, laboratory and pathological factors in 35 females with diffuse proliferative lupus glomerulonephritis were analyzed to determine the prognostic significance of the individual variables. The clinical and laboratory variables were age, serum creatinine (Cr), serum C3, serum C4 and proteinuria at the time of biopsy while the biopsy ones included intraglomerular monocytic infiltration (NSE index), total glomerular deposits, extent of subendothelial deposits, extent of extraglomerular deposits, tubulo-interstitial inflammation, relative tubulo-interstitial volume and total pathologic score. Standard morphometric and counting procedures were used to determine the levels of all pathologic variables but pathologic score and extra glomerular deposits where grading estimates were done. Survival curves were determined by the life table method. Logrank and chi-square tests were used to establish levels of statistical significance. Seven patients developed established renal failure (Cr greater than or equal to 2.0 on two or more occasions at least 3 months apart) and nine showed significant deterioration of renal function (decrease in CrCl of 25% or more in between biopsy and last follow-up visit or an increase in serum Cr of 0.4 mg/dl or more over the follow-up period). The 5-year renal survival rate (absence of established renal failure) for the whole group was 77%. Serum Cr (p less than .005) and extent of extraglomerular deposits (p less than .025) were shown to be significant prognostic factors for renal survival. Of the seven patients who developed renal failure none had an NSE index greater than 3.0 and one had a C3 greater than or equal to 45 mg/dl. Statistically these factors were weak prognostic indicators (0.5 less than p less than .1). Multivariate analysis demonstrated that the extraglomerular deposit factor contributed significant additional prognostic information to that provided by Cr. Although not important as a prognostic factor on its own, the NSE index significantly improved the prognostic performance of serum Cr. The product of the NSE index and serum C3 proved to be a strong prognostic factor (p less than .005).

Adolescent↗

PubMed1984

Monocytes and glomerulonephritis associated with remote visceral infection.

The biopsies of 8 patients with diffuse proliferative glomerulonephritis associated with remote visceral infection (GN-RVI) were evaluated by histochemistry and electron microscopy for the presence and extent of intraglomerular monocytic infiltration. The sites of infection were cardiac valves (2 cases), ventriculoatrial shunts (2 cases), lungs (2 cases), blood (1 case) and retroperitoneal space (1 case). Seven of the patients had an elevated serum creatinine (1.5-6.5 mg/dl) and all had proteinuria, hematuria and an active urinary sediment. Histochemical investigation using the alpha-naphthyl acetate stain for nonspecific esterase (NSE) was conducted in 7 of the biopsies and showed relatively numerous intraglomerular monocytes in 5 cases. Electron microscopy demonstrated conspicuous monocytic infiltration of glomeruli in the 1 biopsy in which histochemistry was not done and in the 5 cases with high NSE indices (mean number of NSE + cells/glomerulus). The mean NSE index for the group was 4.5 (+/- 3.1) (range = 0.6-10.0). This was compared to the mean NSE indices for other types of diffuse proliferative glomerulonephritis (GN) - GN associated with mixed essential cryoglobulinemia (GN-CRY) (4 cases), membranoproliferative GN, type I (MPGN) (18 cases), post-infectious GN (PIGN) (9 cases) and diffuse lupus GN (GN-SLE) (35 cases). The NSE index for GN-RVI was less than that of GN-CRY (9.1 +/- 5.8) but greater than those of PIGN (3.5 +/- 2.5), GN-SLE (2.6 +/- 2.3) and MPGN (1.3 +/- 1.3). The differences between the GN-RVI index and those of GN-CRY, PIGN and GN-SLE were not significant but the difference between GN-RVI and MPGN was (p less than 0.01, Student's test).

Adolescent↗

PubMed1983

Testicular pain: an unusual presentation of polyarteritis nodosa.

We report a case in which the initial presentation of polyarteritis nodosa was alternating bilateral orchialgia. The diagnosis was confirmed by testicular biopsy. Testicular biopsy is an uncommonly reported diagnostic procedure despite the high incidence of testicular involvement in polyarteritis nodosa. We emphasize the value of testis biopsy, particularly when biopsy of other sites does not prove the diagnosis in suspect cases.

Adult↗

PubMed1983

Drug-induced acute interstitial nephritis with granulomas.

To shed more light on the immunopathogenesis of drug-induced acute interstitial nephritis, a combined histologic, immunopathologic, and ultrastructural study of renal biopsy specimens from nine patients with drug-induced renal disease was performed. None of the patients had pre-existing renal disease or evidence of sarcoidosis or tuberculosis. The principal drugs included a hydrochlorothiazide-triamterene combination (Dyazide), hydrochlorothiazide, fenoprofen, and furosemide and triamterene. Renal insufficiency developed approximately four to ten weeks after initiation of drug therapy. In all cases, withdrawal of the drug(s) with or without steroid therapy resulted in restoration of normal or near-normal renal function. Histologically, all biopsy specimens showed acute interstitial nephritis characterized by an intense but patchy mononuclear cell interstitial infiltrate consisting of lymphocytes, monocytes, and plasma cells, modest numbers of eosinophils, patchy tubular atrophy, interstitial edema, and normal glomeruli. All biopsy specimens contained interstitial (and, in two cases, perivascular) non-caseating granulomas, which were numerous in one case, moderate in four cases, and rare in the remainder. Direct immunofluorescence was negative for IgG, IgM, IgA, C1q, C4, and C3 along glomerular and tubular basement membranes. Immunoperoxidase staining for lysozyme (performed in three cases) demonstrated many positive cells in the infiltrate. In two cases in which granulomas were present in prepared sections, the epithelioid and multinucleated giant cells did not stain for lysozyme. Electron microscopy of the granulomas in two cases revealed that the epithelioid and giant cells had "secretory" features characteristic of hypersensitivity granulomas. These findings provide further evidence for the participation of cell-mediated immunity in the pathogenesis of at least some cases of drug-induced acute interstitial nephritis.

Adult↗

PubMed1982

Focal proliferative lupus nephritis. A clinicopathologic study using the W.H.O. classification.

Focal proliferative lupus glomerulonephritis has traditionally been considered to be more benign than the diffuse form. A recent study of lupus nephritis using the W.H.O. classification demonstrated no difference in 4-year survival between those with focal and those with diffuse disease. Because of this development, a comparative clinicopathologic study of 15 patients with focal proliferative lupus glomerulonephritis was done using the W.H.O. classification. Generally, patients with focal proliferative lupus glomerulonephritis presented with milder renal disease with respect to proteinuria and renal insufficiency. Involvement of the central nervous system was more prominent in focal proliferative lupus glomerulonephritis. Therapy for both types of disease was similar. Mean duration of renal disease was 48 months for focal and 50.7 months for diffuse disease. Three patients with focal proliferative lupus glomerulonephritis and two with diffuse proliferative lupus glomerulonephritis were dead at the end of the follow-up period. Established renal failure was present in one patient with focal disease and two with diffuse disease. Deterioration of renal function was noted in two patients with focal proliferative lupus glomerulonephritis and five with diffuse proliferative lupus glomerulonephritis at the end of the follow-up period. No statistically significant differences in cumulative five-year survival rates (focal = 0.751; diffuse = 0.858), cumulative five-year renal survival rates (focal = 1.00; diffuse = 0.846), deterioration of renal function and quantitative proteinuria at the end of the follow-up period were noted. although qualitatively milder, the focal form of renal disease followed a course similar to that of the diffuse type.

Adolescent↗

PubMed1982

Monocyte involvement in glomerular crescents: a histochemical and ultrastructural study.

The biopsies from 14 patients with glomerulonephritis with crescents were studied to determine the extent of monocyte involvement in crescent formation. Antiglomerular basement membrane (GBM) disease was diagnosed in six and immune complex (IC) glomerulonephritis in eight. Alpha-Naphthyl acetate staining of frozen sections for nonspecific esterase was done in 11 cases (five anti-GBM and six IC), and the peroxidase-antiperoxidase method for lysozyme was done in two (both IC). Electron microscopy of crescents was carried out in 12 cases. The mean number of nonspecific esterase (or lysozyme-excluding neutrophils) positive cells was 6.0 (+/-5.8) in the anti-GBM cases and 1.1 (+/- 1.4) in the IC ones. The difference was significant (P less than 0.05). By electron microscopy the cellular crescents in cases of anti-GBM disease contained variable numbers of monocytes (macrophages) and epithelial cells. Those from cases of IC disease showed very few monocytes but numerous epithelial cells. The results show that monocytes participate in a numerically significant way in crescent formation in anti-GBM disease but appear to be of minor importance in crescents in IC disease.

Antibodies↗

PubMed1981

Monocytes and human renal glomerular disease: a quantitative evaluation.

Human renal biopsies (n = 177) were quantitatively evaluated by histochemical means (alpha-naphthyl acetate for nonspecific esterase) for the presence of monocytes within glomerular tufts (excluding crescents). The number of monocytes per glomerulus was counted to obtain the nonspecific esterase index. Histologic, electron microscopic, and direct immunofluorescent features were analyzed. Cases were grouped according to whether intraglomerular electron-dense deposits were present and, if so, their predominant position. Five groups were obtained: group I, subendothelial (39 biopsies); group II, mesangial (24 biopsies); group III, subepithelial (22 biopsies); group IV, intramembranous (2 biopsies); and group V, no detectable deposits (90 biopsies). For each group, the mean nonspecific esterase index was determined: I = 2.0, II = 0.28, III = 0.26, IV = 0.08, and V = 0.13. Group I was subdivided on the basis of whether extensive mesangiocapillary change was present or not. The mean nonspecific esterase index for the group I biopsies without mesangiocapillary change was 2.5, which was significantly higher than the scores for biopsies with mesangiocapillary change (0.2) and those from the other groups (p < 0.01). The results indicate an association between relatively high levels of intraglomerular monocytic infiltration and diseases characterized by having electron-dense immune deposits predominantly in the subendothelial position without extensive mesangiocapillary change. Diseases with predominantly subepithelial, mesangial, intramembranous, or no detectable deposits generally showed low numbers of intraglomerular monocytes.

Esterases↗