scholarly journals A Case Demonstrating the Pathological Relationship between Granulomatous Vasculitis and Glomerular Lesion in Renal Sarcoidosis

2020 ◽  
Vol 10 (3) ◽  
pp. 109-116
Author(s):  
Yoshinori Kamata ◽  
Hiroshi Sato ◽  
Akira Sugiura ◽  
Masahiro Miyata ◽  
Kiyomi Kisu ◽  
...  
Keyword(s):  
Renal Function ◽  
Enzyme Inhibitor ◽  
Oral Prednisolone ◽  
Crescent Formation ◽  
Glomerular Lesion ◽  
Granulomatous Vasculitis ◽  
Glomerular Lesions ◽  
Sclerotic Lesions ◽  
Overt Proteinuria ◽  
Inflammatory Changes

We experienced a rare case of tubulointerstitial angiocentric granulomatous vasculitis with focal segmental glomerulosclerosis (FSGS) and associated sarcoidosis. Our patient was an 18-year-old man who presented with exertional cough and dyspnea. He also had overt proteinuria (3.0 g/24 h), normal renal function (eGFR 95 mL/min/1.73 m<sup>2</sup>), heart failure, and hypertension. He had no previous episode of hypertension. These manifestations immediately improved after the administration of antihypertensive therapy that contained an angiotensin-converting enzyme inhibitor, calcium antagonists, beta antagonists, and diuretics. However, he, later on, developed renal dysfunction, with worsening of both proteinuria and hypertension. Renal biopsy was performed and showed epithelioid cells that were arranged concentrically around small blood vessels in tubulointerstitial granulomas. In the glomeruli, the segmental sclerotic lesions were classified as a perihilar variant of FSGS. There were no inflammatory changes, such as a mesangial lesion, inflammatory cell infiltration, fibrinoid necrosis, or crescent formation, and no glomerular granuloma. In the tubulointerstitial granulomas, the intimal elastic lamina of the interlobular arteries was reduplicated, and the intimal wall thickness of renal arterioles was remarkable. After receiving oral prednisolone therapy, the overt proteinuria resolved, the eGFR recovered from 39.4 to 60.6 mL/min/1.73 m<sup>2</sup>, and hypertension was managed more easily. Thereafter, he did not experience any recurrence. The concurrent improvement of renal function and proteinuria by steroid treatment suggested a relationship between the glomerular lesions and the tubulointerstitial granulomatous vasculitis with associated sarcoidosis.

Organized Intraglomerular Deposits in NZB Mouse Disease

1971 ◽  
Vol 29 ◽  
pp. 544-545
Author(s):  
Francis R. Comerford ◽  
Alan S. Cohen
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Antinuclear Antibodies ◽  
Human Systemic Lupus Erythematosus ◽  
Systemic Lupus ◽  
Glomerular Lesion ◽  
Ultrastructural Studies ◽  
Dense Deposits ◽  
Experimental Nephritis ◽  
Glomerular Lesions

Mice of the inbred NZB strain develop a spontaneous disease characterized by autoimmune hemolytic anemia, positive lupus erythematosus cell tests and antinuclear antibodies and nephritis. This disease is analogous to human systemic lupus erythematosus. In ultrastructural studies of the glomerular lesion in NZB mice, intraglomerular dense deposits in mesangial, subepithelial and subendothelial locations were described. In common with the findings in many examples of human and experimental nephritis, including many cases of human lupus nephritis, these deposits were amorphous or slightly granular in appearance with no definable substructure.We have recently observed structured deposits in the glomeruli of NZB mice. They were uncommon and were found in older animals with severe glomerular lesions by morphologic criteria. They were seen most commonly as extracellular elements in subendothelial and mesangial regions. The deposits ranged up to 3 microns in greatest dimension and were often adjacent to deposits of lipid-like round particles of 30 to 250 millimicrons in diameter and with amorphous dense deposits.

Antihypertensive Property and Renal Protection by Shichimotsu-koka-to Extract in Salt-induced Hypertension in Dahl Strain Rats

1994 ◽  
Vol 22 (01) ◽  
pp. 51-62 ◽  
Author(s):  
Nobuhito Hiwara ◽  
Yoshio Uehara ◽  
Satoru Takada ◽  
Yukari Kawabata ◽  
Nobuko Ohshima ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Aortic Wall ◽  
Antihypertensive Effect ◽  
Blood Pressure Reduction ◽  
Glomerular Sclerosis ◽  
Pressure Reduction ◽  
Renal Protection ◽  
Induced Hypertension ◽  
Sclerotic Lesions

We determined whether or not the kampo formula, Shichimotsu-koka-to extract, attenuates the development of salt-induced hypertension and provides renal protection against hypertensive injury in Dahl salt-sensitive (Dahl S) rats. A six-week treatment using this formula dose-dependently decreased the systolic blood pressure in Dahl S rats fed a high-salt (2% NaCl) diet. This blood pressure reduction was associated with a decrease in the thickness of the aortic wall. Renal function was not altered with this treatment; however, glomerular sclerotic lesions in the kidney were significantly attenuated. Neither arterial nor tubular lesions were affected. These data suggest that Shichimotsu-koka-to extract exhibits an antihypertensive effect which is associated with partial resolution of glomerular sclerosis in the kidney.

scholarly journals Ramipril pretreatment worsened renal injury and survival despite a reduction in renal inflammation in experimentally induced sepsis in mice

2020 ◽  
Vol 21 (2) ◽  
pp. 147032032092397
Author(s):  
Tzvetanka Bondeva ◽  
Katrin Schindler ◽  
Claudia Schindler ◽  
Gunter Wolf
Keyword(s):  
Renal Function ◽  
Enzyme Inhibitor ◽  
Clinical Status ◽  
Cecal Ligation ◽  
Clinical Severity ◽  
Sham Operation ◽  
Cecal Ligation And Puncture ◽  
Renal Inflammation ◽  
Gene And Protein Expression ◽  
Experimentally Induced

Introduction: The angiotensin converting enzyme inhibitor ramipril is a standard antihypertensive therapy for many patients. Because angiotensin II may promote inflammation, we were interested in whether basal pretreatment with ramipril may modify renal function and inflammation as well as systemic outcome in experimentally induced sepsis in mice. Material and methods: Ramipril (10 mg/kg/day) pretreatment or placebo (NaCl) was given intraperitoneally for 5 days to C57BL6/J mice, followed by either sham operation or cecal ligation and puncture sepsis induction. Real-time polymerase chain reaction and immunological stains were used to evaluate renal gene and protein expression, respectively. Plasma creatinine, neutrophil-gelatinase associated lipocalin, and blood urea nitrogen were used as markers for renal function. A clinical severity score was determined. Results: Administration of ramipril before cecal ligation and puncture surgery was associated with reduced renal inflammation but did not improved renal function and structure and even worsened the clinical status of septic mice. Conclusions: The data suggest that the effects of ramipril pretreatment are complex. Additional studies including monitoring of hemodynamic parameters are necessary to elucidate the exact mechanism(s) of this observation. In addition, the timing of the ramipril administration could be of importance.

Glomerular Mesangial Fibrosis in Hatchery-Reared Rainbow Trout (Salmo gairdneri)

1976 ◽  
Vol 33 (11) ◽  
pp. 2551-2559 ◽  
Author(s):  
David E. Hinton ◽  
Raymond T. Jones ◽  
Roger Lee Herman
Keyword(s):  
Rainbow Trout ◽  
Mesangial Cells ◽  
Salmo Gairdneri ◽  
Unknown Etiology ◽  
Electron Microscopic ◽  
Glomerular Lesion ◽  
Ultrastructural Studies ◽  
Glomerular Lesions ◽  
Microscopic Studies ◽  
Rate Comparison

Light and electron microscopic studies were performed on tissues of hatchery-reared rainbow trout (Salmo gairdneri) having a disease of currently unknown etiology with external symptoms of severe edema which causes increased mortality rate. Comparison with unaffected trout tissues revealed loss of cellularity in glomerular tufts with a replacement of mesangial cells by connective tissue. Ultrastructural studies showed the material to be collagen and established the diagnosis of glomerular mesangial fibrosis. The glomerular lesion was associated with alterations in lining epithelium of proximal tubules and extensive debris within tubule lumens. The findings are compared to glomerular lesions in mammalian and amphibian kidney.

Antihypertensive and renal effects of cilazapril and their reversal by angiotensin in renovascular hypertensive rats

1988 ◽  
Vol 74 (4) ◽  
pp. 365-372 ◽  
Author(s):  
Yu-An Ding ◽  
Shin-Tsu Chang ◽  
Shyh-Ming Shieh ◽  
Wann-Chu Huang
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Fractional Excretion ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Renal Effects ◽  
Angiotensin Iii ◽  
Excretion Rates

1. The antihypertensive and renal effects of cilazapril, a new angiotensin converting enzyme inhibitor, were evaluated in both two-kidney, one-clip Goldblatt hypertensive rats (n = 11) and normotensive rats (n = 6). 2. Intravenous infusion of cilazapril (1 mg/kg followed by 25 μg min−1 kg−1) caused significant reductions of blood pressure from 163 ± 3 to 122 ± 4 mmHg and from 157 ± 2 to 113 ± 3 mmHg in two separate groups of hypertensive rats and from 124 ± 1 to 105 ± 2 mmHg in normotensive rats. The hypotensive effect in terms of absolute value or percentage change was greater in hypertensive rats than in normotensive rats (41 ± 6 vs 20 ± 3 mmHg or 25 ± 4% vs 16 ± 2%, respectively). 3. Cilazapril increased glomerular filtration rate, urine flow, and absolute and fractional excretion rates of sodium and potassium in the non-clipped kidney of hypertensive rats. In contrast, the clipped kidney exhibited a depressed renal function during cilazapril infusion. 4. In normotensive rats, the hypotensive and enhanced renal function responses to cilazapril were much less than those of the non-clipped kidney of hypertensive rats. 5. Superimposed administration of either angiotensin II or angiotensin III during cilazapril infusion completely reversed the blood pressure and bilateral renal responses of cilazapril in both hypertensive and normotensive rats. 6. These results indicate that cilazapril reduces arterial pressure and enhances renal excretion mainly via inhibition of angiotensin II and angiotensin III formation.

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