Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated a series of patients with systemic lupus erythematosus (SLE), who had sparse subepithelial and mesangial immune deposits. Our goal was to determine structure: function correlation. We examined whether proteinuria correlated with either capillary wall immune aggregate formation or abnormal podocyte morphology. Renal biopsies from patients with sparse (two or fewer subepithelial or intramembranous electron dense deposits per glomerular capillary loop) immune deposits and podocyte effacement were studied. Patients fulfilled criteria for the diagnosis of SLE. Cases were excluded if the biopsy showed endocapillary proliferation or necrosis. Eighteen biopsies were studied, five from patients with nephrotic range proteinuria (> or =3 g/day) and 13 from patients with non-nephrotic proteinuria (<3 g/day). The five nephrotic patients had a mean foot process effacement of 48% +/- 39% (range 10-100%). Thirteen non-nephrotic patients had a mean foot process effacement of 11.7% +/- 8% (range 0-20%). The only distinguishing morphologic finding associated with nephrotic range proteinuria was diffuse foot process effacement. No correlation between subepithelial deposits and proteinuria was observed. There were no other histologic differences between the nephrotic and non-nephrotic patients. Among these patients, the nephrotic syndrome appears best correlated with podocytopathy rather than subepithelial electron dense deposits, mesangial deposits, or mesangial hypercellularity.
Lupus 2006
PMID:Association of glomerular podocytopathy and nephrotic proteinuria in mesangial lupus nephritis. 1653 76

We describe a 24-year old male patient with systemic lupus erythematosus (SLE) with the gastrointestinal manifestations of protein-losing enteropathy (PLE) and primary sclerosing cholangitis (PSC). He presented with periorbital, scrotal and lower limb oedema. PLE was diagnosed because of hypoalbuminaemia together with an elevation of alpha-1-antitrypsin stool clearance and absence of proteinuria. PSC was diagnosed on the basis of an elevated serum alkaline phosphatase and lymphocytic and fibrous cholangitis. His disease was also complicated by neuropsychiatric lupus and hypogonadism. All the manifestations of SLE resolved with systemic corticosteroids and pulsed cyclophosphamide treatment. This case report documents the unusual association of SLE with PLE and PSC, and this relationship suggests that autoimmunity underlie the pathogenesis of these conditions.
Lupus 2006
PMID:Systemic lupus erythematosus with concurrent protein-losing enteropathy and primary sclerosing cholangitis: a unique association. 1653 81

Management of pregnant women with renal disease involves awareness of, and allowance for, physiological changes including decreased serum creatinine and increased proteinuria. For women with systemic lupus erythematosus (SLE), pregnancy increases likelihood of flare. These can occur at any stage, and are more difficult to diagnose, as symptoms overlap those of normal pregnancy. Renal involvement is no more common in pregnancy. Worsening proteinuria may be lupus flare but differential includes pre-eclampsia. In women with chronic renal disease, pregnancy may accelerate decline in renal function and worsen hypertension and proteinuria, with increased risk of maternal (eg, pre-eclampsia) and fetal (eg, IUGR, IUD) complications, strongly correlating with degree of renal impairment peri-conception. Pregnancy success rate varies from 20% to 95% depending on base-line creatinine. Best outcome is obtained if disease was quiescent for >6 months pre-conception. Women on dialysis or with renal transplants can achieve successful pregnancy but have higher maternal and fetal complication rates. Acute on chronic renal failure can develop secondary to complications such as HELLP and AFLP. Management needs to be by a multidisciplinary team involving physicians and obstetricians, ideally beginning with pre-pregnancy counselling. Treatment of flares includes corticosteroids, hydroxychloroquine, azothioprine, NSAIDs and MME Blood pressure is controlled with methyldopa, nifedipine or hydralazine.
Lupus 2006
PMID:Lupus nephritis and renal disease in pregnancy. 1663 68

A 14-year old girl with lupus erythematosus (LE) who initially showed as discoid lupus and followed with nephrotic syndrome one year later. Concomitant piroxicam and indomethacin were prescribed for her arthritis, which preceded two months before the onset of nephrotic syndrome. Histology from renal biopsy showed minimal-change nephrotic syndrome (MCNS). After continuous treatment for six months, nephrotic syndrome resolved completely and no signs of relapse were noted over 14 years of follow-up. For the children, it is rare to have both LE and MCNS simultaneously; sequela of nonsteroidal anti-inflammatory drugs also seldom results in nephrotic syndrome. Though their relationship is still not defined, the possibility of LE combined with MCNS must be differentiated in patients with lupus and severe proteinuria.
Lupus 2006
PMID:A case of minimal-change nephrotic syndrome in pediatric lupus erythematosus: just a coincidence? 1668 66

Little is known regarding the association of primary antiphospholipid syndrome APLS and proliferative glomerulonephritis GN. We describe a biopsy-documented case with primary APLS and proliferative GN with no evidence of thrombotic microangiopathy TMA, and in the absence of other manifestations of systemic lupus erythematosus SLE. She presented initially with left popliteal deep venous thrombosis and nephrotic syndrome. Her first pregnancy at the age of 26 years resulted in intra-uterine fetal death at term. Two subsequent pregnancies ended up with miscarriages at 3 and 4 months of gestation. Urinalysis revealed glomerular red blood cells of 1.0000.000/ml and granular cast; proteinuria of 13.4 grams/24 hours, which was non-selective; hemoglobin 12 gm/dl, normal white blood cell and platelets; serum albumin 2.6 gm/dl; anti-nuclear antibody ANA and anti DNA were negative and complement levels normal. Lupus anticoagulant was positive leading to a diagnosis of primary APLS. The biopsy findings were consistent with membranoproliferative GN. She continued to have steroid-resistant proteinuria, but stable renal function after a 12-year follow up period. She had 2 pregnancies during this period and was delivered at term using caesarian section. She received heparin during the pregnancies. Later she developed hypertension easily controlled by atenolol. This case provides evidence that primary APLS can be associated with proliferative GN due to immune deposits and not only TMA as previously reported, and in the complete absence of SLE. Performing more renal biopsies in this group of patients may disclose a greater prevalence of proliferative GN and may help in devising a rationale for treatment.
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PMID:Proliferative glomerulonephritis and primary antiphospholipid syndrome. 1683 33

Although multiple studies suggest a potential role for angiotensin II in inflammation, most were performed either in vitro or in animals with non-immune-complex-mediated diseases. Extrapolation of these findings to humans, particularly patients with lupus, which involves multiple immunoregulatory pathways, is unclear. In autoimmune-prone MRL/lpr mice, angiotensin-converting-enzyme (ACE) inhibition improved survival although to a lesser degree than cyclophosphamide and diminished the glomerular histopathologic damage, proteinuria, lymphoid hyperplasia, dermatitis, and hypergammaglobulinemia, with a reduction in TGF-beta1 and beta 2 expression in the kidneys and renal chemokine mRNA expression. Spleen levels of IL-4 and IL-10 were also reduced. Uncontrolled studies in patients with treatment-refractory lupus nephritis showed a significant reduction in proteinuria with ACE-inhibitors and Angiotensin receptor blockers treatment. The 'masking' effect of ACE-inhibitors should be taken into consideration, as an exacerbation of lupus nephritis may be missed when estimated by the magnitude of proteinuria, which is decreased by these treatments. No single ACE genotype was consistently associated with subsets of SLE patients. In retrospective analyses, ACE-inhibitor use predicted a favourable outcome in 94 cases of pauci-immune vasculitis. The attenuating effect of angiotensin II inhibitors on the progression of chronic renal disease is well recognized. The data on the role of this intervention in lupus is limited.
Lupus 2006
PMID:The renin-angiotensin system in lupus: physiology, genes and practice, in animals and humans. 1683 Aug 77

The objective of this study was to identify clinical predictors of response to initial mycophenolate mofetil (MMF) therapy for membranous lupus nephritis (MLN). We observed the clinical outcomes of patients in the Hopkins Lupus Cohort within the first year of initiation of treatment with MMF therapy for newly diagnosed MLN, classified according to the new International Society of Nephrology/Renal Pathology Society (ISN/RPS) 2003 classification. Complete renal remission was defined as proteinuria less than 500 mg/24 hours. Demographic, clinical, treatment and laboratory data were examined for their association with renal remission. Twenty-nine MLN patients treated with MMF were identified. Eleven (38%) patients achieved complete renal remission by 12 months. Of those taking hydroxychloroquine, 7/11 (64%) were in remission within 12 months compared to only 4/18 (22%) of those not on hyroxychloroquine (P = 0.036 based on a log-rank test). This association persisted after controlling for the presence of anti-ds-DNA (P = 0.026). Our results provide evidence that hydroxychloroquine has a benefit for renal remission when MMF is used as the initial therapy for MLN. Although hydroxychloroquine is frequently stopped in patients with lupus nephritis, this study suggests it should be started or maintained.
Lupus 2006
PMID:Hydroxychloroquine use predicts complete renal remission within 12 months among patients treated with mycophenolate mofetil therapy for membranous lupus nephritis. 1683 Aug 83

We performed a prospective study to evaluate the efficacy and safety of low-dose cyclosporine A (CSA) treatment in paediatric lupus nephritis refractory to conventional therapy. Seven children with biopsy-proven Class III-IV lupus nephritis were treated with CSA (2-4 mg/kg/day) combined with low-dose prednisone for one year. All patients had failed to achieve sustained proteinuria remission with corticosteroids and cytotoxic drugs. Proteinuria decreased from median value of 2.5 g/24 hours (range, 1.2-4.9) to 0.14 g/24 hours (range, 0.0-0.84) after treatment (P = 0.018). Median values of creatinine clearance and serum creatinine did not change significantly. Median systemic lupus erythematosus disease activity index score decreased from 12 (range, 6-16) to 4 (range, 0-8) at end of treatment (P = 0.027). However, two patients experienced flares of extrarrenal manifestations and complement levels did not improve. Moreover, most patients relapsed with proteinuria within a few months of stopping CSA therapy. Side effects were not significant. In conclusion, low-dose of CSA combined with steroids appears to be useful to reduce proteinuria in paediatric proliferative lupus nephritis refractory to steroids and cytotoxic drugs; however, relapses are common after CSA discontinuation. Further studies are needed to define the precise role of CSA in paediatric lupus nephritis.
Lupus 2006
PMID:Effect of low-dose cyclosporine A in the treatment of refractory proteinuria in childhood-onset lupus nephritis. 1694

Somatostatin, a naturally occurring neuropeptide, is an immunomodulator which inhibits humoral and cell mediated immunity as well as secretion of proinflammatory cytokines. The objective of this study was to examine the effects of a somatostatin analogue on the severity of glomerulonephritis in the female NZB/W F1 murine model of systemic lupus erythematosus (SLE). Twenty female NZB/W F1 mice were treated at 23 weeks of age with 10 mg/kg of the somatostatin analogue Sandostatin- LAR, IM every four weeks. Ten control mice received IM injection of vehicle. Mice were assessed at four-week intervals for weight change, proteinuria, anti-DNA antibodies and splenocyte cytokine profile. The mice were sacrificed at age 34.5 weeks. Kidneys were collected and evaluated by light and immunofluorescence (IF) microscopy. Spleens were collected and splenocyte intracellular cytokines were measured by FACS analysis. In the treatment group significantly less proteinuria was observed four weeks after the second somatostatin analogue injection (dipstik scale: +2.07 +/- 0.95 versus. +3.5 +/- 1.08, P = 0.0002). The treated mice did not lose weight while the control group lost weight over time (P = 0.016). No differences were noted between the groups in anti-DNA antibody titres, cytokine profile or the severity of lupus nephritis as assessed by light and IF microscopy. Somatostatin analogue treatment attenuated proteinuria and prevented weight loss in NZB/W F1 mice, suggesting a possible beneficial effect on renal parameters and systemic manifestations of the disease. Further studies will be needed to assess the value of somatostatin analogue treatment in lupus nephritis, utilizing higher doses, at different stages of the disease, for longer periods.
Lupus 2006
PMID:Somatostatin treatment attenuates proteinuria and prevents weight loss in NZB/W F1 mice. 1694 6

In an Afro-Caribbean population, 111 new cases of systemic lupus erythematosus were diagnosed in the 10-year period from January 1995. Fifty-three cases (48%) presented with or subsequently developed lupus nephritis (SLEN). We recorded clinical characteristics and treatment outcomes of SLEN. We retrospectively categorized patients into four groups based on presence or absence of proteinuria with or without renal impairment. Group 1 (n = 15, 28%) had normal renal function (creatinine clearance (CrCl) > 70 mL/minute) with urinary protein excretion (UPE) of 0.5-3.0 g/24 hour, group 2 (n = 7, 13%) had normal renal function with UPE > 3.0 g/24 hour, group 3 (n = 9, 17%) had renal impairment (CrCl < 70 mL/minute) with UPE of 0.5-3.0 g/24 hour and group 4 (n = 22, 42%) had renal impairment with UPE > 3.0 g/24 hour. Renal biopsies were performed in 15 patients (28%). The number of treated patients in-remission decreased across the groups, from 100% in group 1 and 71% in group 2, to 33% in group 3 and 32% in group 4 (Pr < 0.001). There were 12 deaths from renal causes: none in groups 1 and 2, two (22%) from group 3 and 10 (45%) from group 4 (Pr = 0.003). In resource-poor clinical settings with limited access to histopathological services, CrCl and UPE may be useful predictors of therapeutic response and clinical outcomes in SLEN.
Lupus 2006
PMID:Lupus nephritis in an Afro-Caribbean population: renal indices and clinical outcomes. 1712 May 98


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