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C Orfila

Publications and source records attributed to C Orfila.

At least 37 records · Page 2Linked to original sources
PubMed1994

Henoch-Schönlein purpura in a patient with diabetic nephropathy.

A 46-year-old man presented with Henoch-Schönlein purpura and diabetic nephropathy. At 30 years of age, the patient had presented with an acute and severe nephritic syndrome with severe renal impairment. The renal function returned to normal 6 months after this first attack. At the age of 38 years, the patient was diagnosed as having type II diabetes and was treated with diet alone. At 44 years of age, a renal biopsy was performed because of proteinuria and hematuria. In this renal biopsy, mesangial expansion, medial arterial hyperplasia, and focal interstitial fibrosis were found to be present. Mesangial and subendothelial deposits of immunoglobulin A (IgA) were demonstrated by immunofluorescence. At 45 years of age, cutaneous vasculitis appeared, and at 47 years of age, the patient presented with necrotic purpura, non-insulin-dependent diabetes, renal impairment, proteinuria, and hematuria. A skin biopsy demonstrated leukocytoclastic skin vasculitis with IgA deposits in the arterial walls. A second renal biopsy was performed that showed diabetic glomerulosclerosis associated with a marked vascular and interstitial fibrosis. Mesangial and subendothelial deposits of IgA and C3 and linear IgG deposits along the glomerular basement membranes were demonstrated by immunofluorescence. Electron microscopy showed that the glomerular basement membranes were thickened; a fusion of foot processes was observed and electron-dense deposits were present in the widened mesangium. In summary, we describe a patient with a history of ancient glomerulonephritis who presented with an IgA mesangial nephropathy consistent with Henoch-Schönlein purpura associated with diabetic glomerulosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 2↗
PubMed1994

[Renal involvement in POEMS syndrome].

We described a patient with a POEMS syndrome (Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal grammapathy and Skin changes) who was found to have renal involvement with peculiar renal pathological findings. Hitherto, 17 other cases, most of them from Japan, of POEMS syndrome with renal involvement, have been published. Clinical features are variable: acute renal failure with anasarca or moderate chronic renal insufficiency with mild proteinuria. This latter presentation often passes unnoticed. There is no severe HTA, no microangiopathic hemolytic anemia. Renal biopsy shows prominent glomerular changes which are unusual and distinct from membranoproliferative glomerulonephritis (MPGN) and from glomerular thrombotic microangiopathy (TMA). Mesangial proliferation and thickening of the capillary wall with double contour evoke by light microscopy a MPGN. By immunofluorescent microscopy, no immunoglobulins or complement deposits are found. The finding of mesangiolytic lesions has led to the term of "mesangiolytic glomerulonephritis". The presence, on electron microscopy, of lucent subendothelial space could evoke TMA. But there is neither thrombi, nor arteriolar changes. We are inclined to presume that microangiopathic lesions are due to chronic injury of glomerular endothelial cells, exacerbated at outbreaks of the disease. An increased production of IL-6 could support the efficacity of corticosteroid therapy, particularly in acute clinical situations.

Adult↗
PubMed1993

Immunolocalization of renal kallikrein-like substance in rat urinary bladder.

The renal origin of kallikrein is now clearly established. However, the presence of kallikrein in urine raises questions about a possible physiological role of this enzyme at the urinary level. We have already demonstrated the presence of kallikrein-like substance in rat ureter. For establishing the continuity of the presence of kallikrein-like substance along the urinary tract we have studied the localization of immunoreactive kallikrein-like substance in urinary bladder of the normal rat by immunohistochemical methods for light- and electron-microscopy, using an antibody against rat urinary kallikrein. By light microscopy, kallikrein-like substance was found to be associated with the lamina propria, which is the connective tissue component which constitutes one layer of the bladder wall. Weak staining was present in the smooth-muscle layer. By immuno-electron microscopy, kallikrein-like substance was localized in fibroblasts which were present in the connective tissue and which penetrated into the layer of smooth muscle; immunoreactivity was observed in endoplasmic reticulum, Golgi apparatus and free polyribosomes. Immunolabelling was demonstrated in no other part of the wall bladder and in no other cellular component. The continuity of the presence of kallikrein-like substance from the kidney to the urinary bladder gives new indications concerning the significance of this system in renal physiology.

Animals↗
PubMed1993

Renal immunolocalization of kallikrein in cisplatin nephrotoxicity in rats.

Treatment of rats with cisplatin (4 mg kg-1 body wt i.p. injection) induced variations of urinary kallikrein excretion (UKE). Three phases were observed: a transient increase of UKE one day after injection, followed by a decrease up to 10 days suggesting an altered biosynthesis and a recovery phase with return to normal control values, 21 days after injection. Early morphological lesions were observed in proximal tubule cells on day 1; severe changes and tubular necrosis were observed in the following days. Less marked changes were also present in distal tubules but the vacuolated and desquamated cells appeared in the lumen of the tubules. By immunocytochemical methods, kallikrein was observed in connecting tubule cells, but also in some proximal tubule cells and along the endothelial side of the glomerular basement membrane and urinary space of glomeruli. An intense labelling was present in desquamated epithelial cells in dilated lumen of tubules. This study provides evidence of the presence of immunoreactive kallikrein in the glomerulus, already reported during acute failure, and confirms the use of urinary kallikrein measurements as a useful non-invasive index to assess a possible nephrotoxic effect at the distal level.

Animals↗
PubMed1993

Rapidly progressive glomerulonephritis associated with bacterial endocarditis: efficacy of antibiotic therapy alone.

A 65-year-old woman presented rapidly progressive glomerulonephritis with purpura and mitral insufficiency. Blood cultures grew Streptococcus mitis. By light microscopy, the renal biopsy revealed necrotizing glomerulonephritis 56% associated with cellular crescents and tubulointerstitial changes. By immunofluorescence, deposits of IgM and C3 were found to be present in the mesangium. Electron-microscopic study showed subendothelial and intramembranous deposits. Treatment with antibiotics alone resulted in renal recovery with disappearance of proteinuria, circulating immune complexes and cryoglobulinemia. A 2nd renal biopsy, performed after 3 months, showed segmental sclerosis and tubulointerstitial lesions. Eight months after the first hospitalization, cardiac insufficiency occurred. Four years later, a valve replacement was performed. No abnormal serum creatinine, serum creatinine clearance or urinalysis levels were present. These data suggest that rapidly progressive glomerulonephritis associated with bacterial endocarditis may be treated by antibiotics alone and result in normal and stable renal function.

Aged↗
PubMed1993

Renal morphological changes after sinoaortic denervation in dogs.

The present study investigates morphological renal lesions in sinoaortic-denervated dogs 1 (n = 6) and 18 (n = 5) months after sinoaortic denervation compared with sham-operated controls (n = 8). After 1 month, a marked hyalinization and moderate thickening of the media of arterioles and small interlobular arteries were observed. These changes associated with edema and intimal thickening led to a narrowing of the lumen. In glomeruli, increase of mesangial matrix was focally present in all cases and associated with mesangial proliferation. In four of six cases, some glomeruli appeared retracted, with a large urinary space. A focal area of interstitial fibrosis occurred in just one case. After 18 months, similar but more pronounced vascular lesions were present, with marked hyperplasia of the media. Glomerular changes were characterized by mesangial lesions associated with focal glomerular sclerosis and thickening of Bowman's capsule. Tubulointerstitial lesions were more prominent in this group, with the presence of tubular epithelial changes and casts. Focal interstitial fibrosis, infiltrates, or both were demonstrated in all cases. These morphological lesions were associated with an increase in arterial blood pressure, proteinuria, and natriuresis and a decrease in urinary kallikrein. These results show that chronic sinoaortic denervation in dogs is associated with renal lesions similar to those observed in other well-established experimental and clinical hypertensive states.

Animals↗
PubMed1992

Evidence for intrarenal kallikrein storage during chromate-induced acute renal failure in rat.

During the course of chromate-induced acute renal failure (ARF), urinary kallikrein excretion (UKE), a serine protease of distal tubule origin in the normal animal was decreased but tissue kallikrein concentration (TK) was increased, suggesting intracellular accumulation. Severe morphological lesions were observed in proximal tubular cells which showed brush border damage, numerous vesicles, necrosis and liquefaction of cytoplasmic material. Less marked changes were also present in distal tubules: large apical vacuoles and swollen mitochondria. Compared to normal rats, using the peroxidase-anti-peroxidase (PAP) method for light microscopy, greater kallikrein immunoreactivity was detected along the apical pole in distal tubules, on the membrane and in the cytoplasm as well as in the glomerulus. By immunoelectron microscopy, kallikrein was found in the connecting apical area, along the luminal, basolateral and basement membranes, in some vesicles, in Golgi apparatus and on ribosomes bound to endoplasmic reticulum. In the glomerulus, kallikrein was observed along the luminal surface of endothelial cell. After 14 days a progressive recovery of renal function, tissue morphology and UKE towards control values was observed. The presence of immunoreactive kallikrein in the glomerulus observed only during ARF confirmed the previous demonstration of kallikrein mRNA in the glomerulus. The cellular accumulation results more likely from a dysfunction of a general secretory mechanism due to cell membrane alteration than from a specific inhibition of kallikrein production and secretion.

Acute Kidney Injury↗
PubMed1991

Distal nephrotoxicity of cisplatin demonstrated by urinary kallikrein excretion and morphological study in rats.

The nephrotoxic effect of cisplatin (4 mg/kg body wt, i.p. injection) was specifically evaluated on the distal tubule. We measured both the tissue concentration and the urinary excretion of kallikrein (UKE), a serine protease mainly synthesized and secreted in the distal connecting tubular cells. In a parallel morphological study, we evaluated the tissue lesions. On the basis of UKE, the three distinct phases of nephrotoxicity were observed. The induction phase, 1 day after cisplatin injection, was associated with a transient increase in UKE. During the maintenance phase, the kallikrein concentration was significantly decreased both in renal cortex and urine for up to 10 days, suggesting an alteration in the biosynthesis with a decrease in the activation of inactive kallikrein. The recovery phase, 21 days after cisplatin injection, was suggested by the incomplete but significant tendency to return towards control values of active UKE. Histological examinations of cisplatin-treated rats showed early lesions of proximal tubules on day 1. The injuries worsened and tubular necrosis was frequently observed on the following days. Distal tubular changes were less marked but vacuolization and desquamation of epithelial cells and swollen and disrupted mitochondria were demonstrated. This study adds new evidence that UKE is a useful and reliable non-invasive index to assess possible nephrotoxic effects in the distal tubule which are also directly visualized by histological lesions.

Animals↗
PubMed1991

Immunotactoid glomerulopathy and cutaneous vasculitis.

A 22-year-old woman presented glomerulonephritis with Schönlein-Henoch-like syndrome and monoclonal abnormality. One month later, she developed a rapidly progressive glomerulonephritis with hypertension and persistent purpura. In the two renal biopsies performed during the first and the second attack, mesangial expansion and thickening of the glomerular capillary walls (associated with 50% of crescents in the second biopsy) were observed on light microscopy. By immunofluorescence faint deposits of immunoglobulins (light and heavy chains) and complement components were found present in the mesangium. Electron microscopy showed tubular microfibrils measuring 19-24 nm in the mesangium, subendothelial and subepithelial areas. A skin biopsy performed during the first attack demonstrated leukocytoclastic skin vasculitis. By immunofluorescence, no deposits were observed. Congo red staining for amyloid and cryoglobulinemia were negative. This case is similar to an entity recently described and named immunotactoid glomerulopathy.

Adult↗
PubMed1991

Fanconi's syndrome, kappa light-chain myeloma, non-amyloid fibrils and cytoplasmic crystals in renal tubular epithelium.

A 59-year-old woman with kappa light-chain myeloma had Fanconi's syndrome characterized by renal glycosuria, generalized aminoaciduria, bicarbonaturia and decrease of phosphorus and uric acid reabsorption. A bone marrow biopsy showed the presence of 27% of dystrophic plasma cells; the cytoplasm of these cells was intensely stained with anti-kappa light-chain monoclonal antibodies. By light microscopy, the renal biopsy revealed a tubulointerstitial nephritis without glomerular lesions and with intratubular casts. By immunofluorescence, no deposits were observed along the glomerular and tubular basement membranes, but a positivity with anti-kappa light chain was noticed in some tubular epithelia and casts. By electron microscopy, fibrils (35-nm diameter) were observed in the cytoplasm of proximal tubular cells. These fibrils were situated in vesicles (100- to 600-nm diameter) in the luminal side of tubular cells. In the basal pole of the cell, fibrils seemed to group in crystals (120- to 200-nm diameter). Only kappa light-chain protein was demonstrated in these fibrils and crystals by an immunoelectron microscopic technique. These data suggested the pathogenic role of the fibrils and crystals present in tubular epithelium in the tubular proximal syndrome.

Bone Marrow↗
PubMed1991

Immunofluorescent deposits on the tubular basement membrane in human renal transplant.

In this retrospective study, the presence of tubular basement membrane (TBM) deposits of IgG and/or C3 was demonstrated in 41 renal transplants (out of 95 studied). The follow-up of these transplants varied from 9 to 19 years. The deposits were of 'linear' type in 9 cases (circulating anti-TBM antibodies were detected in 7 cases by radioimmunoassay tests and/or indirect immunofluorescence), 'granular' type in 22 cases and 'atypical' with linear and granular segments in 10 cases. Light microscopic diagnosis was acute rejection in 26 cases (33 biopsies) associated with deposits along the TBM:linear (6 cases), granular (13 cases) and atypical (7 cases). Chronic rejection present in 15 transplants (21 biopsies) was associated with linear (2 cases), granular (9 cases) and atypical (4 cases) deposits along the TBM. Electron microscopic study of renal tubules showed altered TBM with thickening, lamellation and splitting. Electron-dense deposits were not demonstrated in cases of linear deposits. A long-term follow-up study did not show any difference in survival of transplants presenting acute or chronic rejection associated or not with TBM deposits. If we consider the outcome of the transplants with TBM deposits, those with granular type seemed to have the poorest prognosis at long term, whatever the type of rejection. In the linear TBM deposits group, all the transplant nephrectomies which occurred (7 out of 9 cases) have been performed within 5 years.

Adolescent↗
PubMed1991

Cisplatin nephrotoxicity in cadmium-pretreated rats. Enzymatic, functional and morphological studies.

Treatment of rats with cisplatin or with cisplatin after chronic pre-exposure to cadmium induced a decrease in kidney cytochrome P-450 and glutathione levels, and in glutathione peroxidase and reductase activities. Furthermore, cadmium and cisplatin enhanced lipid peroxidation, oxidized glutathione and N-glucuronyl transferase activity. Glutathione S-transferase (substrate: 1-chloro-2,4-dinitrobenzene) was increased and decreased by cadmium and cisplatin respectively. On morphological observation, cadmium nephrotoxicity was characterized by tubular proximal damage with mitochondrial and lysosomal changes and a widespread vesiculation of tubular cells. A marked focal tubular necrosis associated with cyst formation was observed in cisplatin nephrotoxicity. On the basis of the measured biochemical, functional and histological parameters, it is concluded that cadmium pretreatment did not potentiate the nephrotoxic effect of cisplatin.

Animals↗
PubMed1990

Cisplatin nephrotoxicity in lead-pretreated rats: enzymatic and morphological studies.

Treatment of rats with cisplatin or with cisplatin after chronic pre-exposure to lead induced a decrease in cytochrome P-450, reduced glutathione (GSH), GSH-S-transferase, reductase and peroxidase activities, and an increase in N-glucuronyl transferase, lipid peroxidation and oxidized glutathione (GSSG). On histological examination, rats treated by lead or cisplatin and by lead + cisplatin revealed significant proximal tubular lesions which varied from minimal changes to severe necrosis. Lead toxicity was characterized by irregularity and thickening of glomerular basement membranes, and by tubular mitochondrial alterations associated with the presence of intranuclear inclusions. Cisplatin injury showed more extensive lesions with cellular disorganization. Except for an increase in N-glucuronyl transferase activity, lead did not exert any significant effect on these biochemical and histological parameters and did not significantly modify the deleterious effects of further therapy by cisplatin.

Acute Kidney Injury↗
PubMed1989

Immunohistochemical study of a tubular basement membrane antigen in normal human urinary sediment by a monoclonal antibody.

This preliminary study concerns murine monoclonal antibodies (Mabs) against tubular basement membranes (TBM) of human kidney which were produced by the classical hybridization technique. One of these Mabs (PP8-1) specifically recognized an antigen present in the tubular basement membranes of various portions of tubule and in the Bowman's capsule. By immunocytochemical techniques, this Mab was used to study the presence and the distribution of the related antigen in urinary sediment from 12 normal healthy subjects. This TBM and Bowman's capsule antigen was demonstrated along hyaline urinary cast surface and, in some cases, in free extracellular fibrillar structures morphologically unrelated to the casts. This suggests that, in some normal conditions, catabolism of TBM and/or Bowman's capsule could release material in urine, as it has been described for glomerular basement membrane (GBM) constituents. Such an immunocytochemical approach could be useful to detect components from tubular renal basement membranes in urinary sediment during pathological conditions.

Animals↗
PubMed1989

Inverse relationship between renal and urinary kallikrein during chromate-induced acute renal failure in rat: urinary kallikrein excretion as a possible recovery index.

Acute renal failure (ARF) was induced in rat following a single injection of sodium chromate. A transient polyuria and a 10-fold decrease in glomerular filtration rate was immediately observed after sodium chromate administration. Urinary sodium and potassium excretion were reduced within 24 h and remained decreased for 8 to 10 days. Progressive recovery of normal renal functions, mainly electrolyte excretion and filtration rate was observed 12 days after sodium chromate administration. Urinary kallikrein excretion (UKE) was decreased only 48 h after sodium chromate administration. However the proportion of the active and inactive form excreted was unchanged. UKE remained also at a reduced level for 8 to 10 days and returned progressively to base-line level. The kallikrein content in the tissue was significantly increased immediately after sodium chromate administration and recovered normal values 12 days later. The increase of kallikrein in the tissue is more likely unspecific due to impaired protein transport than a specific stimulation of renal kallikrein biosynthesis. The decreased UKE may indicate a distal tubular reversible dysfunction in this ARF model. These reductions in electrolyte excretion, glomerular filtration and UKE were associated with selective morphological lesions. Whereas the glomeruli were intact, important damages affected proximal tubule cells which appeared necrotic and showed presence of vacuoles, liquefaction of cytoplasmic material and lost of microvilli. Less marked lesions were however observed in distal tubules, particularly large vacuoles were present at the apical poles of the tubule cells, the sites of kallikrein secretion. These distal damages may be involved in the increase of tissue concentration and in the decrease of UKE.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1989

Goodpasture's syndrome with normal renal function.

Two cases of Goodpasture's syndrome with severe pulmonary haemorrhage and normal renal function are described. In spite of minor (patient 2) or even no (patient 1) biological or light microscopic signs of glomerulonephritis, immunofluorescence of immunoglobulin G (IgG) was strongly positive in a linear fashion along the glomerular basement membranes in both patients. We suggest that renal biopsy in patients with apparently idiopathic pulmonary haemorrhage may lead to an early diagnosis of Goodpasture's syndrome. It is not possible in this disease to recognize on presentation those patients who will remit spontaneously and those who will undergo severe disease. The deadly evolution for patient 1 and some cases in the literature lend support to the notion that cytostatics and plasma exchange must be added to corticosteroids, even if pulmonary haemorrhage is not active and renal function is normal at the time.

Adult↗
PubMed1988

Immunofluorescence characterization of light chains in human nephropathies.

Renal tissue from 185 patients with various nephropathies were studied by immunofluorescence, in order to look for the frequency and potential predominance of kappa or lambda light chain glomerular deposits. Four normal renal biopsies were used as controls. An overall study shows that light chains were present in glomeruli in 136 out of 185 cases; kappa light chain deposits were more frequent than lambda light chain deposits (73.5% and 64.3% respectively). An analytical study shows that this was not observed in all nephropathies studied. In mesangial IgA nephropathy, lambda light chain deposits were seen in 81% of cases (29 out of 37) and kappa light chain deposits were observed in 78% (30 out of 37 cases). In lupus nephritis, lambda light chain deposits were present in 13 out of 14 cases (92.8%) whereas kappa light chain deposits were demonstrated in 12 cases (85.7%). In other nephropathies such as membranous, endocapillary proliferative and amyloid nephritis, kappa was the predominant light chain observed in glomeruli or was present in the same number of cases as lambda light chain (mesangiocapillary glomerulonephritis). These findings show that in certain nephritides, for example IgA nephropathy and lupus nephritis, IgA and IgG deposits are mainly composed of lambda light chain in contrast with the normal kappa: lambda ratio in human serum of 2:1.

Basement Membrane↗