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PubMed2001

Renal lesions in leprosy: a retrospective study of 199 autopsies.

In the present work, 199 patients with leprosy who underwent autopsy between 1970 and 1986 were retrospectively studied to determine the prevalence, types, clinical characteristics, and etiologic factors of renal lesions (RLs) in leprosy. Patients were divided into two groups: 144 patients with RLs (RL+) and 55 patients without RLs (RL-). RLs observed in 72% of the autopsied patients were amyloidosis (AMY) in 61 patients (31%), glomerulonephritis (GN) in 29 patients (14%), nephrosclerosis (NPS) in 22 patients (11%), tubulointerstitial nephritis (TIN) in 18 patients (9%), granuloma in 2 patients (1%), and other lesions in 12 patients (6%). AMY occurred most frequently in patients with lepromatous leprosy (36%; nonlepromatous leprosy, 5%; P < 0.01), recurrent erythema nodosum leprosum (33%; P < 0.02), and trophic ulcers (27%; 0.05 < P < 0.10). Ninety-seven percent of AMY was found in patients with lepromatous leprosy, 88% showed recurrent trophic ulcers, and 76% presented with erythema nodosum leprosum. NPS was found in older patients with arterial hypertension, neoplastic diseases, infectious diseases, and vasculitis associated with GN. Most patients with AMY presented with proteinuria (95%) and renal failure (88%). The most frequent causes of death were renal failure in patients with AMY (57%), infectious diseases in patients with GN (41%) and TIN (45%), and cardiovascular diseases in patients with NPS (41%). No difference in survival rates was observed among RL- patients and those with AMY, GN, NPS, or TIN.

Aged↗

PubMed2000

Peritubular capillaries in chronic renal allograft rejection: a quantitative ultrastructural study.

Peritubular capillaries (PCs) with a circumferentially multilayered basement membrane have been suggested as an ultrastructural indicator of chronic renal allograft rejection (CR). The authors validated this lesion as a marker for CR, by analyzing its quantitative features, specificity, and sensitivity in 169 renal biopsy specimens. The mean number of circumferential layers (PCcirc) and the incidences of the grades (mild: 2 to 4, moderate: 5 to 6, severe: 7 or more layers) were investigated in biopsy specimens involving CR (CR(Bx), n = 46), acute rejection (n = 11), normal kidneys (n = 20), psoriatics treated with cyclosporine (n = 13), renal transplants with chronic cyclosporine toxicity (n = 12), native kidney diseases (NKD, n = 56), and transplant nephrectomies attributable to CR (Cr(nephr), n = 11). CR was diagnosed with regard to the clinical features and the presence of intimal fibrosis in 41 biopsy specimens or transplant glomerulopathy in 35 biopsy specimens (cg; identified only by electron microscopy in 10 cases). NKD included chronic glomerulonephritis, chronic tubulointerstitial nephritis, benign nephrosclerosis, thrombotic microangiopathy, diabetic nephropathy, and renal disease in elderly patients (median age, 72 years). All PCs around glomeruli were sampled (median, 14 profiles per case). PCs with a moderate/ severe lesion appeared as serrated profiles with a thick, ribbon-like basement membrane layer in semithin plastic sections. The numbers of circumferentially multilayered PCs were significantly characteristic of CR (PCcirc in CR(Bx): 2.87+/-1.83 SD; range, 0 to 7.36; P < .001 v other groups). A severe lesion occurred exclusively in CR (in 12% of the PCs in CR(Bx), and in 38% in CRnephr). A moderate lesion was observed in 0.6% of the PCs in NKD, 16% in CR(Bx), and 21% in CRnephr. Three or more PCs with a moderate lesion were encountered only in CR. A mild lesion was not suggestive of CR at all. In CR(Bx), 27 cases showed a severe lesion or 3 or more PCs with a moderate lesion (cpc; sensitivity: 59%). Four of the 27 cases lacked cg. The cumulative incidence of cpc and cg was 85%. In transplants with cyclosporine toxicity, the presence of cpc verified the coexistence of CR in 7 specimens. In conclusion, cpc is a specific marker of CR. The incidence of cpc increases as CR progresses. The lesion may be caused by a low-grade rejection injury to the PCs. Careful analysis of semithin sections promotes the better sampling of cpc. An ultrastructural demonstration of cpc and cg defines CR more precisely than does light microscopic evaluation per se.

Adolescent↗

PubMed2005

Involvement of extracellular signal-regulated kinase and p38 in human diabetic nephropathy.

BACKGROUND: The involvement of mitogen-activated protein kinase (MAPK) in human diabetic nephropathy has not been fully investigated. METHODS: The presence of cells positive for the phosphorylated MAPK family (phosphorylated extracellular signal-regulated kinase [p-ERK], phosphorylated p38MAPK [p-p38MAPK]) was investigated immunohistochemically in kidneys of 30 patients with diabetic nephropathy. In addition, 10 patients with minimal change nephrotic syndrome, 10 patients with thin basement membrane disease, and 5 patients with benign nephrosclerosis were studied as disease controls. The presence of activated nuclear factor-kappaB (p65)-positive cells also was evaluated in kidney specimens. RESULTS: In patients with diabetic nephropathy, p-ERK, p-p38MAPK, and p65 were observed in mesangial cells, endothelial cells, podocytes, tubular epithelial cells, and mononuclear infiltrates in interstitium. Numbers of p-ERK-, p-p38MAPK-, and p65-positive cells in both glomeruli and interstitium in patients with diabetic nephropathy were higher than those in controls. In particular, the number of glomerular p-ERK-positive cells in patients with diabetic nephropathy increased in accordance with the progression of glomerular lesions and correlated well with the number of glomerular p65-positive cells (r = 0.654; P < 0.01; n = 30). Conversely, the number of p-p38MAPK-positive cells in glomeruli did not correlate with glomerular lesions. However, the number of tubulointerstitial p-p38MAPK-positive cells in patients with diabetic nephropathy reflected the severity of tubulointerstitial lesions, and numbers of those in the interstitium increased with good correlation to numbers of tubulointerstitial p65-positive cells (r = 0.757; P < 0.01; n = 30) and interstitial CD68-positive macrophages (r = 0.647; P < 0.05; n = 30) and urinary monocyte chemoattractant protein-1 levels (r = 0.605; P < 0.05; n = 30). CONCLUSION: These results suggest that MAPK phosphorylation contributes to human diabetic nephropathy. In particular, ERK and p38MAPK may be distinctly involved in glomerular and tubulointerstitial lesions in human diabetic nephropathy.

Antigens, CD↗

PubMed2001

Renal disease in the inner city.

For various ethnic and socioeconomic reasons the pattern of renal disease in the inner city displays distinctive features. Hypertension is frequent, often intractable, and generally conditioned by salt sensitivity and a high sodium intake. Chronic hypertensive nephrosclerosis, found predominantly in African Americans, comprises marked cardiomegaly, renal shrinkage, and hypertensive retinopathy. It has been overdiagnosed in the past, but actually accounts for less than 20% of end-stage renal disease (ESRD) in African Americans. Malignant hypertension, less frequent nowadays, may cause renal shutdown, which is reversible in a few cases; the heart and kidneys are often of normal size. Idiopathic focal segmental glomerulosclerosis is the most common cause of the primary nephrotic syndrome in blacks, but its incidence has also been rising in whites and Hispanics; it does not respond well to treatment, and almost one half of the patients develop ESRD within 10 years. Systemic lupus erythematosus is also more common in African Americans, in whom the severe proliferative forms of lupus nephritis pursue a more virulent course: one half of such patients develop ESRD in 5 years. Cocaine, the use of which has assumed epidemic proportions, may cause accelerated hypertension, acute renal failure from rhabdomyolysis, and progression of preexisting renal disease. Heroin nephropathy has all but disappeared and has been replaced by human immunodeficiency virus (HIV) nephropathy. The prognosis of HIV-infected patients maintained by dialysis has greatly improved. Sickle glomerulopathy, consisting of mesangial expansion, basement membrane duplication, and the absence of immune deposits, may cause the nephrotic syndrome in 4% of patients with severe sickle cell anemia, heralding death within 2 years in one half of patients and ESRD in two thirds; survival has not improved with dialysis. Diabetes is now the most common cause of ESRD. Familial aggregation of ESRD is frequently encountered. Interventions useful in the general population, such as vascular bypass procedures, should be undertaken with great caution and restraint in dialysis patients.

Female↗

PubMed2001

Cocaine use and chronic renal failure.

Urban communities vary from suburban and rural communities in several ways, which are reflected in a modified risk for different causes of chronic renal disease. Many rural communities are more similar to urban communities in regard to socioeconomic adversities, access to health care, and other related challenges. It is important to recognize that high population density is commonly associated with a unique set of cultural practices including higher rates of perceived stress, recidivism and incarceration, and substance abuse. Each of these may predispose to higher rates of selected renal disorders such as hypertensive nephrosclerosis, human immunodeficiency virus (HIV) nephropathy, and substance abuse-associated renal disease. Having an understanding of urban culture and lifestyle can increase the awareness of potential contributing factors to chronic renal failure (CRF) in this population and assist in developing screening programs for high-risk individuals, considering specific diagnoses that may not be readily apparent and implementing effective early treatment.

Adult↗

PubMed1987

Long-term results of surgical and conservative treatment of patients with primary aldosteronism.

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.

Adrenalectomy↗

PubMed2005

[Lymphoproliferative disease following kidney transplantation].

HISTORY AND CLINICAL FINDINGS: A 31-year-old male patient was referred because of a worsening graft function 56 months after an allogenic kidney transplantation for interstitial nephritis. He had complained about diffuse abdominal pain and watery diarrhea during the preceding week. Correction of volume status did not result in an improvement of kidney function. Bacterial or viral enteritis could be excluded as well as a mucosa-associated lymphatic tissue lymphoma (MALT-lymphoma). Shortly thereafter, the patient developed a subileus. INVESTIGATIONS: Kidney biopsy showed a low degree nephrosclerosis and some interstitial fibrosis, but no signs of rejection. The abdominal CT scan showed enlarged lymph nodes partially obstructing the intestinal lumen. Histology showed an EBV-negative, highly aggressive B-blastic lymphoma. DIAGNOSIS: EBV-negative post-transplant lymphoproliferative disease (PTLD). TREATMENT AND COURSE: Because of the advanced lymphoma stage immunosuppressive therapy was reduced and immunochemotherapy according to the CHOP-protocol (cyclophosphamide, doxorubicin, vincristine, prednisone) in combination with rituximab (R-CHOP) was started. After 4 chemotherapy cycles the patient was in complete remission and another 2 therapy cycles were given for consolidation. The patient remained free of disease during the actual follow-up of 8 months. CONCLUSION: PTLD can present with unspecific abdominal symptoms including diarrhea and with signs of graft dysfunction.

Abdominal Pain↗

PubMed1998

[Primary Sjögren's syndrome and glomerulonephritis].

HISTORY AND CLINICAL FINDINGS: An 82-year-old woman with hypertension for 20 years developed a nephrotic syndrome with severe oedema followed by acute oliguric renal failure after a bout of bronchitis and a gastrointestinal infection. She also complained of xerostomia and dry eyes of recent onset. INVESTIGATIONS: Biochemical tests showed a serum creatinine level of 6.1 mg/dl, a 1:5120 antinuclear antibody (ANA) titre, and positive values for Ro(SS-A) and La(SS-B) antibodies. HLA-DR typing demonstrated HLA-DR3 (HLA-DRB1*0301) and DR13 (HLA-DRB1*13) antigens. Renal biopsy revealed minimal glomerular lesions with focal and segmental glomerulo-sclerosis as well as (hypertension-induced) benign nephrosclerosis and focal tubular atrophy with interstitial fibrosis. TREATMENT AND COURSE: After two hemofiltrations and concomitant administration of 100 mg prednisone renal function quickly improved and the proteinuria fell to 1 g/dl. At the same time the xerostomia improved. The nephrotic syndrome recurred 7 months later after the prednisone dose had been reduced to 10 mg/d, but after the dose had been raised to 50 mg/d and cyclosporin A (150 mg/d) had been added a lasting remission occurred and renal function became stable though impaired. CONCLUSION: The relatively rare association of glomerular disease (here focal segmental glomerulosclerosis) with Sjögren's syndrome can, as in this case, be triggered by a viral infection. A genetic predisposition for Sjögren's syndrome is suggested by the demonstration of HLA-DR3 alleles. Administration of steroids is indicated for the treatment of the nephrotic syndrome and, in case of recurrence, can be combined with cyclosporin A. Both drugs also influence the symptoms of Sjögren's syndrome.

Aged↗

PubMedDate not supplied

[Tetra-X syndrome with epilepsy, mental retardation and multiple dysmorphias].

It is reported on a 21-year-old female with super-female syndrome in association with an early childhood brain damage exhibiting idiopathic epilepsy, severe oligophrenia, emotional instability, Little syndrome, areflexia of the legs, strabismus, telecanthus, broad nose, epicanthic fold, clinodactyly of little fingers, radio-ulnar-synostosis, retardation of ossification, aortic insufficiency, erythro-cyanosis, one-side clubfoot and nephrosclerosis, also menstrual cycle dysfunction.

Abnormalities, Multiple↗

PubMed1986

[Comparison of the renal ultrasound-furosemide test with the isotope nephrogram. Possible clue to the retention phenomenon?].

In 23 patients with essential hypertension renographic and sonographic examination of the kidneys was compared. No correlation could be observed for functional parameters and urinary excretion between the two different methods. Correlations have only been detected between renographic retentions and furosemide-conditioned swelling of the kidneys in sonography: patients with severe retention showed a statistically significant stronger response to furosemide. The increased retention in the renal pelvis could be responsible for alterations in sonographic findings. This study provides new data on the mechanisms of retention, whereby retention in the renal pelvis in some patients seems to be most probably caused by nephrosclerosis.

Adult↗

PubMed1983

Racial differences in plasma high-density lipoproteins in patients receiving hemodialysis. A possible mechanism for accelerated atherosclerosis in white men.

Among 346 nondiabetic patients receiving long-term hemodialysis, cardiovascular mortality was higher in white than in black men (P less than 0.02) but was similar between black and white women, despite the higher incidence of nephrosclerosis in black men and women (59 and 58 per cent vs. 8 and 10 per cent, respectively; P less than 0.0001). There were significant racial differences in plasma lipid and apoprotein levels in a subset of 100 of these patients. The white men had higher levels of plasma triglyceride and lower levels of high-density-lipoprotein (HDL) cholesterol, apoprotein A-I, and apoprotein A-II than black men; concentrations of HDL, apoprotein A-I, and apoprotein A-II were also lower in white than in black women. The distribution of the HDL subfractions HDL2, HDL3, and HDL3D, as determined by zonal ultracentrifugation, was normal in black and abnormal in white men receiving hemodialysis. HDL2 concentrations were higher in black than in white men by both zonal analysis (P less than 0.05) and polyanionic precipitation of the HDL subfractions (P less than 0.01). The distributions and concentrations of HDL2 and HDL3L were similar in black and white women. Thus, there are marked racial differences in HDL in male patients receiving hemodialysis. The abnormalities in HDL and the hypertriglyceridemia in the white men may explain their high rate of cardiovascular mortality.

Adult↗

PubMed1995

Apoptosis and loss of renal tissue in polycystic kidney diseases.

BACKGROUND: Polycystic kidney disease is characterized by the enlargement of renal cysts, interstitial fibrosis, and gradual loss of normal renal tissue in association with progressive deterioration of renal function. The process causing the progressive loss of renal tissue is unknown, but it could be the result of a form of programmed cell death known as apoptosis. METHODS: We assayed apoptotic DNA fragmentation in normal and polycystic kidneys biochemically by gel electrophoresis and histochemically by in situ end-labeling. A DNA-specific dye, Hoechst 33258, was used to detect morphologic apoptosis in renal samples from patients with normal kidneys, polycystic kidney disease, and other kidney diseases. RESULTS: Apoptotic DNA fragmentation was detected in polycystic kidneys from 5 patients without renal failure and 11 patients with renal failure but not in kidneys from 12 patients with no renal disease. In situ end-labeling revealed apoptotic cells in glomeruli, in cyst walls, and in both cystic and noncystic tubules of the polycystic kidneys. No tubular apoptosis was detected in renal-biopsy specimens from five patients with IgA nephropathy, three patients with nephrosclerosis, two patients with focal glomerulosclerosis, one patient with diabetic nephropathy, six patients with acute tubular necrosis, or four patients with acute and four patients with chronic renal-transplant rejection. The capacity of polycystic kidney cells to undergo apoptosis was retained in vitro in the absence of uremia, ischemia, and other confounding pathologic conditions. CONCLUSIONS: Apoptotic loss of renal tissue may be associated with the progressive deterioration of renal function that occurs in patients with polycystic kidney disease.

Animals↗

PubMed1996

Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency. The Angiotensin-Converting-Enzyme Inhibition in Progressive Renal Insufficiency Study Group.

BACKGROUND: Drugs that inhibit angiotensin-converting enzyme slow the progression of renal insufficiency in patients with diabetic neuropathy. Whether these drugs have a similar action in patients with other renal diseases is not known. We conducted a study to determine the effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of renal insufficiency in patients with various underlying renal diseases. METHODS: In a three-year trial involving 583 patients with renal insufficiency caused by various disorders, 300 patients received benazepril and 283 received placebo. The underlying diseases included glomerulopathies (in 192 patients), interstitial nephritis (in 105), nephrosclerosis (in 97), polycystic kidney disease (in 64), diabetic nephropathy (in 21), and miscellaneous or unknown disorders (in 104). The severity of renal insufficiency was classified according to the base-line creatinine clearance: 227 patients had mild insufficiency (creatinine clearance, 46 TO 60 ml per minute), and 356 had moderate insufficiency (creatinine clearance, 30 to 45 ml per minute). The primary end point was a doubling of the base-line serum creatine concentration or the need for dialysis. RESULTS: At three years. 31 patients in the benazepril group and 57 in the placebo group had reached the primary end point (P<0.001). In the benazepril group, the reduction in the risk of reaching the end point was 53 percent overall (95 percent confidence interval, 27 to 70 percent), 71 percent (95 percent confidence interval, 21 to 90 percent) among the patients with mild renal insufficiency, and 46 percent (95 percent confidence interval, 12 to 67 percent) among those with moderate renal insufficiency. The reduction in risk was greatest among the male patients; those with glomerular diseases, diabetic nephropathy, or miscellaneous or unknown causes of renal disease; and those with base-line urinary protein excretion above 1 g per 24 hours. Benazepril was not effective in patients with polycystic disease. Diastolic pressure decreased by 3.5 to 5.0 mm Hg in the benazepril group and increased by 0.2 to 1.5 mm Hg in the placebo group. CONCLUSIONS: Benazepril provides protection against the progression of renal insufficiency in patients with various renal diseases.

Adult↗

PubMed2000

Neurohormonal modulation in cardiovascular disease.

The renin-angiotensin system (RAS) is one of the oldest known hormone systems. Its effector hormone, angiotensin (Ang) II, acts through 2 receptor subtypes, AT(1) and AT(2). Most physiologic effects of Ang II, including vasoconstriction, renal salt and water retention, aldosterone and vasopressin release, and sympathetic facilitation, are mediated by AT(1). Recent data, however, suggest that Ang II also contributes to cell proliferation, left ventricular hypertrophy, vascular media hypertrophy, neointima formation in atherosclerosis, and nephrosclerosis by stimulation of AT(1) receptors. AT(2) receptors are associated with antiproliferation, cell differentiation and development, tissue regeneration, and apoptosis. They also antagonize AT(1) receptor-mediated effects, which suggests that the ratio of angiotensin receptors expressed on a particular cell can determine the net effect of Ang II. Selective AT(1) receptor antagonists ("sartans") have been used to treat several million hypertensive patients worldwide. These agents offer a powerful therapeutic alternative to angiotensin-converting enzyme (ACE) inhibitors, which reduce the generation of Ang II. Conversely, AT(1) receptor antagonists block the RAS by acting on cellular angiotensin receptors and do not interfere with the breakdown of kinins. These medications inhibit the RAS more completely than do the ACE inhibitors because their action is independent of Ang II-generating pathways. At the same time, early, preliminary data suggest that AT(1) receptor antagonists offer target-organ protection similar to that provided by the ACE inhibitors. Because AT(2) receptors are left unopposed and Ang II levels are increased with AT(1) receptor antagonist treatment, it is important to understand the function of AT(2) to fully appreciate the mechanisms of action of AT(1) receptor antagonists, especially their potential for target-organ protection.

Angiotensin II↗

PubMed1994

Advanced glycation end products induce glomerular sclerosis and albuminuria in normal rats.

High levels of tissue advanced glycation end products (AGEs) that result from the spontaneous modification of proteins by glucose occur in diabetes and aging. To address the potential pathogenic role of AGEs in the glomerulosclerosis of diabetes or nephrosclerosis of aging, doses of AGE-modified rat albumin (25 mg per kg per day, i.v.) sufficient to elevate circulating AGE levels to the range of diabetic serum were administered daily to healthy rats alone or in combination with the AGE inhibitor aminoguanidine. After 5 months, the AGE content of renal tissues in AGE-treated rats rose to 50% above controls (P < 0.025), whereas serum contained 2.8-fold greater AGE levels (P < 0.025). Light and electron microscopy of kidneys from AGE-treated rats revealed a more than 50% increase in glomerular volume compared to controls (P < 0.001), significant periodic acid/Schiff reagent-positive deposits, basement membrane widening, and mesangial extracellular matrix increase and indicated significant glomerulosclerosis compared to untreated (P < 0.002) or albumin-treated controls (P < 0.002). These changes were associated with significant loss of protein (P < 0.005) and albumin (P < 0.002) in the urine of AGE-treated rats compared to controls. Cotreatment with aminoguanidine markedly limited both the structural and functional defects. These in vivo data demonstrate that AGEs influence glomerular structure and function in a manner leading to glomerulosclerosis. The effects are AGE-specific, as they are ameliorated by a pharmacological AGE inhibitor, aminoguanidine.

Aging↗

PubMed2004

Renal replacement therapy in Sweden.

OBJECTIVE: The Swedish Registry for Active Treatment of Uraemia (SRAU) was founded in 1991 with the objective of documenting demographic data on patients treated for end-stage renal disease (ESRD). The aim of this study was to describe the prevalence, incidence, comorbidity risk factors and survival of patients with ESRD who underwent dialysis treatment and/ or kidney transplantation in Sweden between 1991 and 2002. MATERIAL AND METHODS: All dialysis and transplant units (n = 65) presently report to the SRAU and almost all patients are reported and followed until death. RESULTS: The prevalence of patients on dialysis and transplantation, being approximately 750 per million population (PMP), has increased by 75% in 12 years. The recent annual rise is approximately 3% (200 patients). The incidence has been stable since 1997 at approximately 125 patients PMP. In 2002, there were 1113 new patients, the majority of whom were aged > or =65 years. Their original kidney disease was most often diabetic nephropathy (23.7%), with nephrosclerosis (19.0%) being the second most common disease. The total number of renal transplantations performed has decreased to some extent. The overall 5-year patient survival rate was 23.1% in patients on dialysis and 85.5% after kidney transplantation. The major cause of death was cardiovascular disease (48%) and an increasing frequency of malignancy after transplantation (26%) was noted. CONCLUSION: The prevalence of ESRD has nearly doubled since 1990 and the number of new patients being referred for dialysis has increased. These patients are becoming older, with a large proportion having non-renal complicating diseases. Survival after transplantation was excellent. The shortage of cadaveric donors in Sweden in recent years and increasing mortality from malignant disease after transplantation are issues of great concern.

Adolescent↗

PubMed2002

Angiotensin receptor antagonists in patients with nephropathy due to type 2 diabetes.

In the past few years diabetes has become the leading cause of end-stage renal disease in all Western countries. A correlation between blood pressure and rate of progression in diabetic nephropathy was noted very early, and increased local activity of the renin angiotensin system was identified as a major pathophysiological mechanism for proteinuria and nephrosclerosis in diabetic patients. Angiotensin converting enzyme (ACE) inhibitors have been shown to slow progression of nephropathy in type 1 diabetic patients. The majority of diabetic patients with nephropathy, however, are suffering from type 2 diabetes and until last year there was no convincing evidence of ACE inhibitors being able to slow progression in type 2 diabetic patients with nephropathy. Three new studies now fill this gap, showing that angiotensin receptor blockers (ARB) are nephroprotective in patients with type 2 diabetes, independently of blood pressure. This review provides an in-depth discussion of the results of these studies and provides recommendations for patient management.

Angiotensin II↗

PubMed2003

Angiotensin AT1/AT2 receptors: regulation, signalling and function.

Angiotensin II (Ang II), the biologically active component of renin-angiotensin system (RAS), acts through two receptor subtypes, the AT1 and the AT2 receptor. All classic physiological effects of Ang II, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. Ang II, via its AT1 receptor, is also involved in cell proliferation, left ventricular hypertrophy, nephrosclerosis, vascular media hypertrophy, endothelial dysfunction, neointima formation and processes leading to athero-thrombosis. Recent investigations have established a role for the AT2 receptor in cardiovascular, brain and renal function as well as in the modulation of various biological processes involved in development, cell differentiation, tissue repair and apoptosis. This review summarizes new insights in the regulation, signalling and (patho-) physiological functions of AT1 and AT2 receptors. An extensive review on angiotensin receptors has been published recently (de Gasparo M et al., Pharmacol Rev 2000; 52: 415-72).

Angiotensin II Type 1 Receptor Blockers↗