Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of angiotensin converting enzyme inhibitors (ACEIs) along with good blood pressure control have been shown to significantly decrease the level of proteinuria and slow the progression of renal insufficiency in patients with nondiabetic glomerular disease including focal segmental glomerulosclerosis (FSGS). Thus, this should be part of the therapeutic approach for all proteinuric patients with FSGS and should be considered the mainstay of therapy for patients with FSGS secondary to conditions associated with hyperfiltration and/or reduced nephron mass and those patients with nonnephrotic primary FSGS. However, nephrotic patients with primary FSGS may continue to have marked proteinuria and progression of renal disease despite these measures and thus require a more aggressive approach with the use of steroids and immunosuppressive agents. Although primary FSGS was once thought to be a steroid-nonresponsive lesion, recent experience has provided a note of optimism in the use of steroids and immunosuppressive agents in treating this otherwise progressive glomerulopathy. As a result, a course of steroid therapy in primary FSGS is now warranted in nephrotic patients with reasonably well preserved renal function in whom it is not otherwise contraindicated.
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PMID:Angiotensin antagonists and steroids in the treatment of focal segmental glomerulosclerosis. 1270 83

Histopathological features of transplanted kidneys which gradually lose graft function have been traditionally reported with the term of chronic rejection (CR). In 1997 Banff's classification indicated the adoption of a new term for all these histological features, namely Chronic allograft nephropathy (CAN), recommending that the presence of morphological aspects suggestive of chronic rejection, such as chronic transplant glomerulopathy (CTG) and proliferative endoarteritis (PE), has to be specified. On the basis of these criteria we reviewed the renal biopsies of 92 patients who underwent kidney transplantation from 1999 to 2002. In all cases the biopsy had been performed 6 months after organ transplantation. In 30 of the 92 patients CTG and/or PE was evident supporting a diagnosis of CR; on the contrary, in 11 of the 92 patients the final diagnosis based on histological evidence was that of CAN. Clinical and laboratory tests revealed that the presence of proteinuria in patients with CR at the time of diagnosis was the single statistically significant difference between these two groups. In 7 of the 32 patients where the diagnosis of CR was based on the presence of early features of CTG, the treatment with ACE-I induced complete remission of the proteinuria. Cyclosporine-induced arteriolopathy (CSA) represents an additional histological finding which has been associated with graft loss in the transplanted kidney. The observation of arteriolopathy, similar to CSA in patients who did not receive calcineurine inhibitors, suggests some caution in the use of this diagnostic criteria.
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PMID:[Clinical anatomical features of chronic dysfunction in the transplanted kidney]. 1573 43

Diabetic nephropathy (DN) is characterized by glomerulopathy and tubulointerstitial expansion followed by renal fibrosis. Angiotensin II (Ang II) and connective tissue growth factor (CTGF) are involved in the pathogenesis of DN, while Janus kinase 2 (JAK2) is important in advanced glycation end-product (AGE)-induced effects in renal interstitial (NRK-49F) fibroblasts. Thus, we studied the role of Ang II, CTGF, and JAK2 in AGE-induced effects in NRK-49F cells. We found that AGE (150 microg/ml) increased mitogenesis and type I collagen production at 7 days while Ang II (10(-7)M) increased mitogenesis and type I collagen production at 3 days. We also found that AGE (150 microg/ml) increased angiotensinogen protein at 2 days, which was attenuated by AG-490 (a JAK2 inhibitor). AGE (150 microg/ml) increased CTGF mRNA and protein expression at 3 and 5 days, respectively. Ang II (10(-7)M) increased CTGF mRNA and protein expression at 1 and 2 days, respectively, which were attenuated by AG-490. Moreover, losartan (a type I angiotensin receptor blocker) and captopril (an angiotensin converting enzyme inhibitor) attenuated AGE-induced CTGF mRNA/protein expression while attenuating AGE-induced mitogenesis and type I collagen production. AG-490 and CTGF antisense (but not sense) oligodeoxynucleotide (ODN) attenuated Ang II (10(-7)M) and AGE-induced mitogenesis and type I collagen production at 3 and 7 days, respectively. We concluded that AGE (150 microg/ml)-induced mitogenesis and type I collagen production are dependent on the Ang II-JAK2-CTGF pathway in NRK-49F cells. Moreover, Ang II-induced mitogenesis and type I collagen production are dependent on the JAK2-CTGF pathway.
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PMID:Advanced glycation end-product-induced mitogenesis and collagen production are dependent on angiotensin II and connective tissue growth factor in NRK-49F cells. 1577 Jun 49

Excess body weight may be associated with various functional/structural lesions of the kidney. The spectrum ranges from glomerulomegaly with or without focal or segmental glomerulosclerosis, to diabetic nephropathy, to carcinoma of the kidney and nephrolithiasis. The first sign of renal injury is microalbuminuria or frank proteinuria, in particular in the presence of hypertension. The occurrence of microalbuminuria and/or chronic kidney insufficiency (glomerular filtration rate < 60 mL/min/1.73 m2) is related to the increasing number of components of the metabolic syndrome, ie, central obesity, elevated fasting blood glucose level, hypertriglycerides, low high-density lipoprotein cholesterol, and hypertension. In the long run, end-stage renal failure may develop. An increased body mass index is particularly harmful in patients with reduced renal functional mass (unilateral renal agenesis or nephrectomy) and other renal diseases (immunoglobulin A nephritis and chronic graft dysfunction after kidney transplantation). In the pathogenesis of obesity-associated glomerulopathy, hyperfiltration is of fundamental importance. The factors involved are energy intake (high protein and salt), hyperinsulinemia, and enhanced tubuloglomerular feedback because of increased sodium reabsorption. The adrenergic and renin-angiotensin-aldosterone systems as well as glucocorticoids are stimulated. In addition, several active proteins generated in the central adipose tissue, such as leptin, proinflammatory cytokines, plasminogen activator inhibitor-1, angiotensinogen, and growth factors (transforming growth factor-beta1), as well as low levels of the protective adiponectin, may contribute to renal injury. Of greatest importance is the development of hypertension and of diabetes, which are directly related to the severity of central obesity. Obesity-associated renal disease should be prevented or retarded by weight reduction following lifestyle modification (salt restriction, hypocaloric diet, aerobic exercise), or eventually by antiobesity medication or bariatric surgery. In the presence of glomerulopathy and/or hypertension, angiotensin converting enzyme inhibitors or angiotensin II type I receptor blockers are the drugs of choice to improve glomerular hyperfiltration.
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PMID:Renal disease in obesity: the need for greater attention. 1682 23

Clinical and experimental diabetic states are often characterized by an increase in the glomerular filtration rate, and early hyperfiltration may be a risk factor for the later development of diabetic glomerulopathy. Evidence in diabetic animal models suggests that, of the determinants of diabetic hyperfiltration, glomerular capillary hypertension plays a key role in the development of structural injury. In diabetic rats, despite normal systemic blood pressure, the glomerular capillary pressure is elevated because of disproportionate vasodilation of the afferent arteriole. In this normotensive model, a modest reduction in systemic blood pressure with angiotensin I-converting enzyme inhibitor therapy normalizes glomerular capillary pressure and retards the development of injury. However, animal studies suggest that all antihypertensive regimens may not afford equivalent protection. It has been reported that monotherapy with calcium channel blockers, or hydralazine, is less effective in limiting albuminuria than are angiotensin-converting enzyme inhibitors. In a study comparing the effects of angiotensin-converting enzyme inhibitors with those of reserpine, hydrochlorothiazide, and hydralazine, both regimens lowered blood pressure and offered some long-term protection. However, angiotensin-converting enzyme inhibition resulted in significantly greater limitation of injury than did the combination regimen. These results suggest that antihypertensive therapy retards diabetic renal disease; however, some anti-hypertensive regimens may afford superior protection.
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PMID:Effects of angiotensin-converting enzyme inhibitors in experimental diabetes. 1698 65

Epidemiological studies have proven that obesity is a significant risk factor for type 2 diabetes. Long-term progression of diabetes leads to various microvascular complications, of which diabetic nephropathy has become of increasing importance, and is the main cause of end-stage renal failure in occidental countries. Microalbuminuria is the first marker of incipient diabetic nephropathy, an early stage glomerulopathy which can progress to renal failure and which historically has been treated with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists. We report a severely obese diabetic patient on treatment for diabetic nephropathy with ACE-inhibitors and poor results, which resolved after Roux-en-Y gastric bypass.
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PMID:Resolution of early stage diabetic nephropathy in an obese diabetic patient after gastric bypass. 1705 53

We present the case of a 22-year-old male with chronic hepatitis B virus (HBV) infection, who developed nephrotic syndrome and had complete remission after lamivudine monotherapy. Renal biopsy showed membranous glomerulopathy, and the serum titer of HBV DNA increased to 1,130,000 copies/mL. As symptomatic therapy with angiotensin converting enzyme inhibitors did not improve the nephrotic syndrome, lamivudine 100 mg per day was started. His alanine aminotransferase level normalized 2 months after treatment, then hepatitis B e antigen seroconversion developed and serum HBV DNA became undetectable. His proteinuria improved subsequently and his leg edema disappeared completely 6 months after treatment. Neither hepatitis nor nephrotic syndrome had relapsed by month 13 when he came for follow-up. This suggests that lamivudine monotherapy may induce and maintain complete remission of membranous glomerulopathy associated with hepatitis B.
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PMID:Complete remission of nephrotic syndrome of hepatitis B virus-associated membranous glomerulopathy after lamivudine monotherapy. 1796 68

Diabetic nephropathy is an important cause of morbidity and mortality in patients with either type 1 or type 2 diabetes mellitus. The pathogenesis and natural history of diabetic nephropathy, characterised by a progressive decline in glomerular function, were initially described in patients with type 1 diabetes. Reports that describe the glomerulopathy and progression of renal disease in patients with type 2 diabetes suggest that the disease process is similar to that observed in patients with type 1 diabetes with diabetic nephropathy. An emerging body of evidence supports the notion that glomerular capillary wall and mesangial alterations in diabetic nephropathy involve pathobiochemical alterations of glycoproteins in these structures. Evidence in experimental animals rendered diabetic, reveal that the administration of heparin and other anionic glycoproteins can effectively prevent the biochemical alterations that promote albuminuria. Clinical reports of the use of sulodexide, a preparation of low molecular weight glycosaminoglycan polysaccharides, have shown that proteinuria is significantly diminished in patients with diabetic nephropathy, even when these patients are receiving either an ACE inhibitor or angiotensin receptor antagonist.
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PMID:The role of sulodexide in the treatment of diabetic nephropathy. 1806 18

Paraneoplastic glomerulopathies are rare manifestations of neoplastic disease to be distinguished from iatrogenic renal damage. Solid tumors are preferentially associated with membranous nephropathy, whereas Hodgkin's lymphomas are associated with minimal change disease. The most common neoplasia associated with paraneoplastic glomerular disease are carcinomas of the lung and of the gastrointestinal tract. Nephrotic syndrome is the most frequent presentation of paraneoplastic glomerulopathy and the most critical glomerular disease regarding prognosis and patient care. Renal biopsy is recommended in patients with glomerular proteinuria or nephrotic syndrome and cancer, depending on life expectancy and therapeutic options. The primary treatment must be directed at the cancer in all cases. Symptomatic treatment of the nephrotic syndrome with diuretics and ACE inhibitors is justified. Prevention of nephrotic syndrome complications, i.e. thromboses and infections, should also be addressed and systematic regular renal follow-up is warranted. All treatments should be regularly reviewed to avoid toxicity, associated renal function loss or low albumin levels for patients receiving albumin-binding drugs. Epidemiologic studies have low evidence-based value. There is no widely accepted experimental model of the association of glomerulopathy and cancer. Thus, epidemiologic and mechanistic studies are needed to determine the true prevalence of paraneoplastic glomerulopathies and investigate new pathophysiologic approaches.
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PMID:Paraneoplastic glomerular diseases and malignancies. 1879 Jun 51

Systemic erythematosus lupus (SLE) is a multisystemic autoimmune disease which has nephritis as one of the most striking manifestations. Although it can coexist with other autoimmune diseases, and determine the predisposition to various infectious complications, SLE is rarely described in association with non-lupus nephropathies etiologies. We report the rare association of SLE and primary IgA nephropathy (IgAN), the most frequent primary glomerulopathy in the world population. The patient was diagnosed with SLE due to the occurrence of malar rash, alopecia, pleural effusion, proteinuria, ANA 1: 1280, nuclear fine speckled pattern, and anticardiolipin IgM and 280U/mL. Renal biopsy revealed mesangial hypercellularity with isolated IgA deposits, consistent with primary IgAN. It was treated with antimalarial drug, prednisone and inhibitor of angiotensin converting enzyme, showing good progress. Since they are relatively common diseases, the coexistence of SLE and IgAN may in fact be an uncommon finding for unknown reasons or an underdiagnosed condition. This report focus on the importance of the distinction between the activity of renal disease in SLE and non-SLE nephropathy, especially IgAN, a definition that has important implications on renal prognosis and therapeutic regimens to be adopted in both the short and long terms.
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PMID:IgA nephropathy in systemic lupus erythematosus patients: case report and literature review. 2726 46


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