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Biomedical subjects

M Susin

Publications and source records attributed to M Susin.

At least 55 records · Page 3Linked to original sources
PubMed1984

Experimental focal segmental glomerulosclerosis: correlation with protein excretion, glomerular filtration rate, and renal plasma flow.

A rat model of focal segmental glomerulosclerosis (FSGS) produced by repeated injections of aminonucleoside (AMN) of puromycin was used to evaluate the relative roles of hemodynamic alterations and AMN-induced glomerular visceral epithelial cell injury in the development of FSGS. Twenty rats received three intraperitoneal injections of AMN on days 1, 21, and 28 and developed significant proteinuria. On day 50, 14 rats (group 1) underwent selective left renal perfusion with AMN and six rats (group 2) received left renal perfusion with saline. At sacrifice on day 70 or 110, group 2 rats had similar values in left and right kidneys for glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and the amount of FSGS (13.1 +/- 5.6% in left and 12.9 +/- 7.8% in right). In contrast, group 1 rats manifested a significantly higher amount of FSGS in right kidneys as compared to left kidneys (3.1 +/- 1.3% in left and 6.3 +/- 2.0% in right, as well as significantly diminished GFR and ERPF in left as compared to right kidneys. A higher degree of FSGS was seen in kidneys with a higher GFR and ERPF. A positive correlation was observed between the mean 24-h protein excretion of the rats and the percentage of FSGS in left and right kidneys (r = 0.66, p less than 0.01).

Animals↗
PubMed1984

Pulmonary sequestration.

Pulmonary sequestration is a disturbance in embryonic development that results in a cystic mass of nonfunctioning lung tissue. The authors present a case of this disorder and review the pertinent literature.

Adult↗
PubMed1983

Biclonal IgM gammopathy in a lymphoproliferative disorder.

An unusual case of an IgM producing lymphoproliferative disorder is presented. Using immunofluorescent techniques, this study shows that the heavy chain is associated with kappa light chain in some cells, and with lambda light chain in other cells. This indicates the presence of two distinct malignant cell populations in this patient.

Aged↗
PubMed1983

Fibrillary renal deposits and nephritis.

Fibrillary renal deposits and nephritis. The authors have studied 8 patients whose glomeruli contain abundant fibrils in their mesangial matrix and basement membranes. Although the location of these fibrils is very similar to that of amyloid, they are about twice the size of amyloid fibrils, averaging 20 nm in width, and fail to react as amyloid does with special stains. Immunofluorescence-microscopic studies are usually positive with antiserums to IgG, often IgM, and in some cases IgA, and also kappa and lambda light chains, C3, and C4. The fibrils are associated with diffuse mesangial widening and increased mesangial matrix strands. Although peripheral glomerular capillary walls appear to be spared initially, their eventual involvement leads to glomerular capillary collapse and glomerular obsolescence. Crescent formation occurred in 5 cases, focally in 3 and diffusely in 2. Tubular basement membrane involvement was seen in 1 case. These patients exhibit hematuria, and proteinuria, and often hypertension and renal insufficiency. Proteinuria was in the nephrotic range in 3 patients in whom involvement of glomerular capillary basement membranes was extensive. Unless electron microscopy is applied to renal biopsies, these cases may be considered to represent mesangiocapillary or rapidly progressive glomerulonephritis, or amyloidosis. The nature of these fibrils is as yet not determined. It is likely that they have been called "atypical amyloidosis" in the past.

Adult↗
PubMed1982

PUlmonary embolism Low incidence in chronic renal failure.

The records of 2,255 autopsies performed on adults between Jan 1, 1969, and Dec 31, 1981, were reviewed for the presence of pulmonary embolism. The overall incidence was 32.3% (18.4%, microscopic; 4%, microscopic; and 9.9%, both). During this period, 95 patients with chronic renal failure (serum creatinine level, greater than 5.0 mg/dL) were identified. The incidence in this group was 9.47% (all microscopic). We conclude that pulmonary embolism is an infrequent cause of mortality in patients with chronic renal failure.

Adolescent↗
PubMed1981

Recurrent nephrotic syndrome with three successive renal allografts.

A girl with idiopathic steroid-resistant nephrotic syndrome was studied at onset of the disease at 6 years of age and during recurrences of the nephrotic syndrome after successive transplantations of three renal allografts. Focal glomerulosclerosis was demonstrated shortly after onset of the original disease with progression to renal insufficiency over 14 months. Recurrence of the nephrotic syndrome was documented 4 weeks following transplantation of the first renal allograft and a biopsy demonstrated focal segmental glomerulosclerosis without evidence of rejection. By 13 months, recurrent disease had caused renal failure requiring dialysis. After transplantation of the next long-functioning graft, the nephrotic syndrome rapidly recurred with urinary protein excretion of 8 g/day and normal glomerular filtration rate at 8 weeks. After the 5th month, progressive renal insufficiency developed and dialysis was resumed at 10 months after transplantation. The nephrectomy specimen showed advanced focal segmental glomerulosclerosis and chronic rejection. Early after the last renal allograft, she had mild persistent proteinuria and then developed nephrotic syndrome at 10 months which was attributed to chronic rejection. The graft was lost to delayed accelerated rejection at 17 months. The rapid recurrence of nephrotic syndrome after transplantation of each of the first two long-functioning allografts to this patient is most consistent with recurrence of original disease. However, observations in a subsequent graft demonstrated that rapid recurrence of the original disease is not inevitable.

Adolescent↗
PubMed1981

Does treatment of hypertension prevent renal failure?

The association between malignant hypertension and renal insufficiency is now well established. The previous adage of not treating this entity for fear of precipitating renal failure has now been replaced by one of aggressive medical therapy as a means to prevent further renal damage. Even when treatment appears to cause renal insufficiency, continued aggressive therapy is indicated as the majority of these people will either stabilize or even improve their renal function. The association of renal failure and benign hypertension is less clear. We feel that if long-term controlled studies could be performed, benefit would be evident. However, even without this evidence, the ability to prevent the malignant hypertensive lesion is sufficient reason to aggressively treat this group.

Animals↗
PubMed1981

Cellular schwannoma: a variety of schwannoma sometimes mistaken for a malignant tumor.

Fourteen cellular schwannomas, a variety of peripheral nerve sheath tumor showing a predominantly compact cellular growth, no formed cellular palisades or Verocay bodies, but the ultrastructure of schwannomas, are reported. A presumed nerve of origin was identified in three instances. The tumor had no sex predeliction; the mean age was 48. The neoplasm is usually well encapsulated and most commonly presents in the neck, posterior mediastinum, or pelvis. Because of a variety of confusing histologic features, including dense cell bundles and fascicles, storiform areas, a moderate mitotic activity and moderate nuclear atypia, six of 14 cases were mistaken for either fibrous histiocytoma, leiomyoma, malignant peripheral nerve sheath tumor, or sarcoma of uncertain type. In two instances the false impression of a malignant tumor was reinforced by clinical evidence of bony erosion and destruction. Follow-up thus far has shown the tumor to be benign.

Adult↗
PubMed1980

Meningeal involvement in IgD myeloma with cerebrospinal fluid paraprotein analysis.

Myelomatous meningitis is a rare occurrence in multiple myeloma. We report 2 cases of documented IgD myeloma with cytologic evidence of meningeal involvement in 1 and detailed paraprotein analysis in both. The occurrence of meningeal involvement in this rare form of plasma cell neoplasm may be more common than previously thought.

Aged↗
PubMed1980

Nephrotic syndrome and multiple tubular defects in children: an early sign of focal segmental glomerulosclerosis.

The nephrotic syndrome is rarely associated with renal tubular defects, and the combination has been reported only in association with advanced renal insufficiency. We report here five children with nephrotic syndrome and multiple tubular defects which evolved when glomular filtration rate ranged between 56 and 90 ml/minute/1.73 m2. The tubular defects were first noted at 3, 4, 4, 7, and 22 months after the onset of the nephrotic syndrome, and renal glycosuria was the first sign in all five children. Glycosuria was intermittent in three patients, constant in two, and ceased with loss of kidney function. Four patients had hyperaminoaciduria and renal tubular acidosis (two of four tested had distal renal tubular acidosis). Three patients had decreased tubular reabsorption of phosphorus and defective maximum concentrating capacity. All five had focal segmental glomerulosclerosis proven by renal biopsy. Over a follow-up period of seven years, all of the children have developed advanced renal insufficiency, four of the five have required dialysis or transplantation within 21 to 72 months after onset, and one has stabilized renal function at 35 ml/minute/1.73 m2. The one patient receiving a kidney transplant has had recurrence of focal segmental glomerulosclerosis in the transplanted kidney and became nephrotic with three subsequent transplants. Our experience suggests that the nephrotic syndrome associated with tubular defects in children forms a subgroup of focal segmental glomerulosclerosis, with rapid progression to renal insufficiency and the potential for recurrence of the lesion in the transplanted kidney.

Acidosis, Renal Tubular↗
PubMed1980

Kidney transplant nephrotic syndrome: relationship between allograft histopathology and natural course.

We analyzed clinical and pathologic data from 36 recipients of 38 renal allografts who developed nephrotic syndrome following transplantation. Three groups were identified on the basis of histologic changes in the graft, and each group had a distinct clinical course. Nine grafts (23.7%) had recurrent glomerulonephritis (GN) (5 membrano-proliferative, 4 focal glomerulosclerosis) and developed nephrotic syndrome at 5.1 months (mean) posttransplant. Renal function deteriorated rapidly, with a 2-year graft survival of 29.7%. Four grafts (10.5%) with de novo GN (3 epimembranous, 1 minimal change) developed nephrotic syndrome at 32 months posttransplant, and all functioned for more than 3 years. Twenty-five grafts (65.8%) had allograft glomerulopathy with the onset of nephrotic syndrome at 9.1 months posttransplant and a 2-year graft survival of 66.6%. The differences in duratin of graft function between grafts with allograft glomerulopathy and recurrent GN (P < 0.01) and in graft survival rates at 2 years among the three groups (P < 0.05) are statistically significant. This analysis indicates that allograft glomerulopathy is the most common cause of kidney transplant nephrotic syndrome. Membranoproliferative GN and focal glomerulosclerosis may recur soon after transplantation and rapidly progress to renal failure in marked contrast to grafts with either de novo epimembranous nephropathy or minimal glomerular change, lesions that are compatible with prolonged graft function.

Adolescent↗
PubMed1980

Mesangial electron-dense deposits in membranous nephropathy.

In the absence of lupus, mesangial electron-dense deposits in membranous nephropathy are thought to be uncommon. In this study 18 renal biopsies of 16 cases seen over a 2-year period were evaluated by light and electron microscopy and immunofluorescence, directing particular attention to the mesangium. Lupus had been excluded in every instance by the usual serologic tests. In seven of the 18 biopsies, mesangial electron-dense deposits were found. Clinically, almost all of these patients were characterized by atypical features: five patients had underlying diseases which have been associated with membranous nephropathy (renal vein thrombosis, epidermoid carcinoma of the lung, SH-antigenemia, rheumatic heart disease and penicillamine therapy); there was one instance of spontaneous remission and another patient who progressed to terminal renal failure in less than 2 years. The results suggest that the presence of mesangial deposits in membranous nephropathy may be more common than has previously been suspected. This finding is not necessarily associated with systemic lupus erythematosus and may indicate an unusual or atypical form of membranous nephropathy.

Adolescent↗
PubMed1977

Presacral myelolipoma: report of a case and review of the literature.

A benign presacral tumor composed of adipose and hematopoietic tissue was found in an asymptomatic 47-year-old woman. Due to the patient's associated medical conditions the tumor was diagnosed by transanal biopsy and was not removed. Only three similar cases have been reported.

Female↗
PubMed1977

Focal glomerular sclerosis.

There seems to be little doubt that FGS is a nonspecific lesion that represents one way in which the renal glomerulus responds to a variety of injuries. This is illustrated by the large number of diverse conditions with which the lesion is associated including various forms of glomerulonephritis, pyelonephritis, hereditary nephritis, and heroin usage. Nevertheless, there remains a relatively large isiopathic group which, though possibly heterogeneous, displays a number of characteristic clinical and pathologic features including the following: 1. Steroid-resistant nephrotic syndrome; 2. Hematuria and hypertension; 3. Normal serum complement; 4. Progressive renal insufficiency; 5. Typical pathologic lesion most common in or restricted to juxtamedullary cortex; 6. Absence of clearly defined evidence of immune complex deposition by immunofluorescent or electron microscopic studies; 7. Recurrence of the lesion following renal transplantation. The pathogenesis of these changes is unclear, the evidence for an immune complex mechanism meager, and the suggestion that the disease is mediated by a humoral mechanism remains to be explored. The potential recurrence of this lesion in the transplanted kidney affords a unique opportunity to study the disease early in its course by a variety of techniques that may help to clarify this still poorly understood entity.

Basement Membrane↗