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Biomedical subjects

B C Sturgill

Publications and source records attributed to B C Sturgill.

At least 37 records · Page 2Linked to original sources
PubMed1987

Immunoglobulin light chain nephropathies.

Excessive monoclonal light chain production and excretion may result in a variety of renal diseases which may collectively or individually be referred to as light chain nephropathy. Kappa light chains are more likely to produce tubular dysfunction and nodular nonamyloidotic glomerulosclerosis, while lambda light chains are more likely to be involved in the development of amyloidosis. The physicochemical reasons for this segregation are poorly understood. Affected patients may present with minor tubular dysfunctions, acute or chronic renal failure, mild proteinuria, or severe nephrotic syndrome. Underlying each is a dyscrasia of plasma cells or frank multiple myeloma with excessive production of monoclonal light chains. Electron microscopy and immunofluorescence studies of renal biopsies have been critical in defining these nephropathies and continue to be essential in establishing the diagnosis.

Amyloidosis↗
PubMed1986

Progression of membranous nephropathy to acute crescentic rapidly progressive glomerulonephritis and response to pulse methylprednisolone.

There have been only sporadic reports of membranous nephropathy (MN) evolving into acute crescentic rapidly progressive glomerulonephritis (AC-RPGN). A patient with MN developed acute oliguric renal failure with a serum creatinine (SCr) of 8.4 mg/dl after 5 years of normal renal function. Biopsy now revealed epithelial crescent formation superimposed on MN. Pulse methylprednisolone resulted in significant improvement in renal function, with a SCr of 2.2 mg/dl at 6 months. No other favorable outcomes occurred in the 4 previous case reports of MN evolving into RPGN. AC-RPGN should be considered a treatable etiology of acute renal failure in the setting of MN.

Acute Kidney Injury↗
PubMed1985

Congo red-negative amyloidosis-like glomerulopathy.

Three cases of amyloidosis-like glomerulopathy are presented in which renal amyloidosis was initially diagnosed on the basis of ultrastructural findings, despite negative Congo red staining. The histologic and immunofluorescence findings and, on careful examination, ultrastructural features of this amyloidosis-like glomerulopathy all serve to distinguish it from true amyloidosis. The clinical behavior suggests that it is a primary glomerulopathy since, with time, no other systems become involved.

Adult↗
PubMed1985

Isolated xanthomatosis of the small bowel.

A case of xanthomatosis of the small bowel is described. Beginning with the proximal jejunum, an 85-cm segment of small bowel was distorted by regularly spaced nodular accumulations of lipid-laden macrophages that expanded the submucosa and muscularis and extended to the serosal surface. The conditions often associated with xanthomatosis were not found in this patient.

Humans↗
PubMed1985

Ultrastructural studies of experimental autoimmune glomerulonephritis in normal and bursectomized chickens.

Immunizations of chickens with bovine glomerular basement membrane (GBM) results in the development of experimental autoimmune glomerulonephritis (EAG). Animals lacking antibody to GBM develop nephritis comparable to those with antibody. The present study examined the ultrastructural lesions of EAG. Normal and bursectomized (Bsx) chickens were immunized with complete Freund's adjuvant (CFA) or CFA-GBM. We studied 3 CFA controls, 5 CFA-Bsx controls, 5 GBM immunized, 4 Bsx-GBM immunized antibody positive birds, and 6 Bsx-GBM immunized birds with no antibody. Ultrastructure of control animals was consistent with previous descriptions in chickens. In nephritic GBM-immunized animals the proliferative glomerulonephritis was associated with an increase in resident mesangial (type I) cells identified by small regularly shaped nuclei with coarsely clumped chromatin and scanty cytoplasm. (p less than 0.05). Glomerulonephritis was also associated with the occurrence of type II cells characterized by an irregular folded lobulated nucleus, finely granular chromatin, abundant cytoplasm, and dense granules and vacuoles in the cytoplasm with an appearance similar to macrophages. The presence of type II cells was highly associated with the development of glomerulonephritis, p less than 0.05. The increase in type II cells was observed in animals with and without antibody along the GBM. A third type of cell was also observed in intimate contact with type II cells and had the morphology of a lymphocyte. The lymphocytoid cells were only seen in nephritic animals. Bsx was associated with trabeculation and lucencies of the GBM not found in normal birds, p less than 0.05. EAG in chickens occurs regardless of the presence or absence of GBM-bound anti-GBM antibody. Other studies have shown that the disease can be transferred by specifically sensitized lymphocytes, but not by antibody. The present ultrastructural findings provide further evidence for the role of cell mediated immunity in the pathogenesis of this model of EAG in chickens.

Animals↗
PubMed1984

Bladder polyp and heavy proteinuria in a patient with Hodgkin's disease in remission.

A 21-year-old man who developed heavy proteinuria 8 years after remission of Hodgkin's disease treated with MOPP chemotherapy and radiation therapy is reported. Evidence of Hodgkin's disease could not be documented, and minimal changes were revealed by renal biopsy. Proteinuria persisted for 20 months and was followed by dysuria and the discovery of an inflammatory polyp of the bladder. The proteinuria decreased 1 month after excision of the polyp, and disappeared during the following year. Rather than indicating relapse of lymphoma, proteinuria in this patient resulted from a lesion not previously associated with Hodgkin's disease, but possibly resulting from long-term effects of therapy.

Adult↗
PubMed1984

Cold-reactive alloantibodies and allograft malfunction occurring immediately posttransplant.

Certain kidney allografts function promptly, whereas others subjected to similarly optimal procurement and preservation methods do not. Previous reports have indicated that such unexplained allograft malfunction (AM) could be due to the presence of cold-reactive IgM alloantibodies (i.e., lymphocytotoxins and agglutinins) present in renal transplant recipients. These investigations were undertaken to determine whether the presence of such alloantibodies was associated with any histological abnormalities. Pretransplant and 1-hr posttransplant biopsies were analyzed from 49 cadaveric renal allografts that came from ideal donors and were subjected to "optimal" preservation. First, no correlation could be made between AM and the severity of renal tubular cell disruption. However, glomerular lesions in the posttransplant biopsy correlated significantly with the development of AM. Segmental glomerular intracapillary red blood cell aggregates and fibrin deposition were present in 71% of biopsies in the 21 allografts with AM, whereas such lesions were present in 29% of biopsies in the 28 allografts with immediate function (P less than 0.005). Development of glomerular lesions correlated significantly with the presence of cold-reactive lymphocytotoxins (CRL) in the recipient (60% vs. 9%). Sera containing CRL were found to also have IgM antiendothelial cell antibody. These observations suggest that another possible mechanism for lack of prompt allograft function is a self-limiting vascular injury, that occurs in the cold and is immune-mediated.

Antilymphocyte Serum↗
PubMed1984

Cold-reacting IgM antibody-induced renal allograft failure. Similarity to hyperacute rejection.

Hyperacute rejection of renal allografts is usually mediated by IgG antibody, but recent studies indicate that cold-reacting IgM alloantibodies are also associated with immediate malfunction of renal allografts. We report 2 cases of cold-reacting IgM-mediated allograft malfunction in which immediate posttransplant biopsies resembled hyperacute rejection. This reaction can probably be prevented by warming the kidney just before transplantation.

Acute Disease↗
PubMed1984

New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

The present study examined the role of cell-mediated immunity (CMI) in the production of experimental autoimmune glomerulonephritis (EAG) in chickens deficient in humorally mediated immunity (HMI). Cyclophosphamide bursectomized (Bsx) and normal control chickens were used. Bsx chickens were used only if they had severe depression of HMI, which was evidenced by marked reduction in bursal weights (0.89 +/- 0.23 vs. 2.92 +/- 0.9 g), decreased serum IgG to less than or equal to 10% of normal, and total lack of HMI to immunization with sheep red blood cells. EAG was produced by immunizing chickens with bovine glomerular basement membrane (GBM) in complete Freund's adjuvant. CMI manifested by wattle thickness increments to PPD was not different, 3.89 +/- 0.45 mm for Bsx compared with 3.73 +/- 0.75 mm for controls. No circulating antibodies to GBM developed in 68% of Bsx chickens, and the anti-GBM titers were less than 1:312 in those Bsx chickens positive for antibody compared with greater than 2,000 for controls. GBM deposits of IgG by fluorescence were much decreased, 0.53 +/- 0.16 compared with 2.19 +/- 0.32 for controls, and were absent in 64% of Bsx chickens. Nonetheless, proliferative nephritis with crescents was present and was even more severe in Bsx chickens than in controls, with glomerular sizes of 20.8 +/- 0.6 U for Bsx-GBM, 19.8 +/- 1.2 for control-GBM, 14.9 +/- 1.5 for Bsx, and 13.6 +/- 0.8 for normal chickens. Nephritic eluates did not produce disease in normal chickens, while administration of sensitized cells with [H3]thymidine to naive birds was associated with increased mesangial grain counts by autoradiography. These findings suggest that CMI plays a major role in the pathogenesis of EAG in chickens in the absence of HMI. By implication, CMI may be crucial in the development of other types of glomerulonephritis as well.

Animals↗
PubMed1984

Early onset of clinical diabetic nephropathy in children--a new subgroup?

The onset of fixed proteinuria and hypertension in insulin-dependent diabetic is generally associated with eventual renal insufficiency due to diabetic nephropathy or with a superimposed glomerulopathy. We report three adolescents with normal renal function who developed fixed proteinuria and hypertension after only 7 to 11 years of insulin-dependent diabetes mellitus. Blood pressure ranged from 130/95 to 165/104 mmHg, urinary protein excretion was 1.31 to 1.37 g/24 hours, and creatinine clearance ranged from 98-133 ml/min/1.73 m2. Renal biopsy revealed changes consistent only with diabetic glomerulosclerosis. Follow-up evaluation for 11 months to 3 1/2 years revealed blood pressure reductions to 125/78-140/85 mmHg as a result of antihypertensive medications. Creatinine clearance increased by 12-20% and urinary protein excretion remained unchanged. We conclude that these patients may represent an unusual subgroup of insulin-dependent diabetics with early development of clinical and pathological diabetic nephropathy in the face of normal renal function.

Adolescent↗
PubMed1983

Membranous glomerulopathy and nephrotic syndrome after captopril therapy.

Membranous glomerulopathy and proteinuria have occurred in patients receiving captopril for hypertension. In this case of captopril-associated nephrotic syndrome, a pretreatment biopsy specimen showed normal histologic appearance and glomerular ultrastructure. A posttreatment biopsy specimen showed membranous glomerulopathy. It seems likely that captopril caused the membraneous glomerulopathy.

Biopsy↗
PubMed1982

Prolonged anuria and aortic insufficiency in a child with Wegener's granulomatosis.

A 16 year-old boy developed generalized Wegener's granulomatosis with rapidly progressive renal insufficiency resulting in prolonged anuria. He was treated with cyclophosphamide, prednisone and anticoagulants, and was maintained on peritoneal dialysis for seven weeks, after which he regained a GFR of 35 ml/min. Recovery of renal function following prolonged anuria has not been previously reported in a child with Wegener's granulomatosis. The patient also developed aortic regurgitation, a cardiac lesion not previously described in this disorder.

Adolescent↗