Development Of End-stage Renal Failure Research Articles

The Early Diagnosis and Treatment of Chronic Renal Insufficiency.

Chronic renal insufficiency (CRI) is becoming more common and has an increasing impact on public health. In Germany, approximately one in ten adults has CRI. Its most serious consequence is generally not the development of end-stage renal failure, but rather the markedly increased cardiovascular risk as kidney function declines. This review is based on the findings of a selective search in PubMed for literature about the treatment options for CRI, and on our overview of the existing guideline recommendations on diagnostic testing. . Patients with diabetes mellitus and arterial hypertension are at especially high risk of developing CRI. For these patients, some of the guidelines recommend regular testing for albuminuria and measurement of the glomerular filtration rate (GFR), though sometimes only when specific risk constellations are present. The treatment of CRI has evolved in recent years. At first, aside from general measures, only RAS inhibitors were available as a specific therapy for CRI. With the extension of the approval of SGLT-2 inhibitors to non-diabetic CRI patients, the options for treatment have become wider. Two randomized controlled trials have revealed the benefit of SGLT-2 inhibitors with respect to their primary combined endpoints: time to a specified eGFR reduction and renal/cardiovascular death (HR 0.61 [0.51; 0.72] and 0.72 [0.64; 0.82]). The potential side effects and contraindications of SGLT-2 inhibitors must be taken into account. A further treatment option for diabetics with CRI has become available with the approval of the non-steroidal mineralocorticoid receptor antagonist finerenone. In patients with risk factors, renal function should be regularly tested.

Arterial hypertension as a risk factor for the development of CKD in children with CAKUT syndrome and its correction

The review is devoted to the development of end-stage renal failure (ESRD) in children with congenital anomalies of the kidneys and urinary tract (CAKUT syndrome. In this regard, measures to slow the progression of chronic kidney disease (CKD) are important. One of the independent risk factors for a decrease in excretory renal function is arterial hypertension (AH), the correction of which is a mandatory component of nephroprotection. CAKUT syndrome is associated with a congenital decrease of the mass of active nephrons, which inevitably leads to hyperfiltration, the main cause of the development of ESRD has a high prevalence in CACUT syndrome and plays a special role in maintaining hyperfiltration. The presence of cysts, nephrosclerosis sites, and endothelial dysfunction contribute to the activation of renin secretion with a further increase in the role of the renin-angiotensin-aldosterone system (RAAS). Angiotensin II is not only a powerful vasoconstrictor. Its effects on sympathetic stimulation of dense spot, hyperplasia of smooth muscle cells, increased expression of several growth factors, cytokines and chemokines is known. The result of the interaction of this complex is the development of glomerular hypertrophy, tubulointerstitial inflammation and fibrosis. Blood pressure correction should begin with lifestyle modification. It is recommended to start taking antihypertensive drugs in children with blood pressure > 90 percentile. Among the first-line pharmacological drugs for the treatment of hypertension, angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin II type I receptor blockers (ARBs) play a major role. Unlike adults, a combination of them is possible.

АУТОСОМНО-ДОМИНАНТНАЯ ПОЛИКИСТОЗНАЯ БОЛЕЗНЬ ПОЧЕК С ОЧЕНЬ РАННИМ НАЧАЛОМ

Both autosomal dominant polycystic kidney disease and autosomal recessive polycystic kidney disease may occur at any age starting infancy and up to adulthood. Manifestations of autosomal dominant polycystic kidney disease usually occur in adult patients with a risk of development of end-stage renal failure after the fifth decade of life. However, an increase in the number of pediatric cases of a very-early onset of the disease, in utero or during the first 18 months of life, had been registered recently, that were characterized by severe clinical manifestations which in tis turn had mimic the autosomal recessive polycystic kidney disease. The three infant cases of autosomal dominant polycystic kidney disease are observed in the Article with perinatal period features, clinical manifestations of the disease, tests’ results and its interpretation given. Children with very-early onset of autosomal dominant polycystic kidney disease are in the high-risk group for nephromegaly, severe hypertension and the early end-stage renal failure.

#5499 COULD MESANGIAL C3 DEPOSITION BE AN INDEPENDENT PROGNOSTIC MARKER IN IMMUNOGLOBULIN A NEPHROPATHY?

Abstract Background and Aims Immunoglobulin A nephropathy (IgAN) is a common primary glomerulonephropathy and the role of complement activation in the pathogenesis has not been fully clarified. There is evidence that mesangial C3 deposition plays a role in the development of the disease. The aim of this study was to examine the effect of C3 deposition on the prognosis of IgAN patients. Method The study included 1135 patients with IgAN confirmed by biopsy using the datatbase of the Turkish Nephrology Association Glomerular Diseases Working Group (TSN-GOLD). Patients were excluded from the study if they were aged <18 or >75 years, or if C3 staining had not been performed in the immunofluorescent analysis. C3 deposition was defined as immunofluorescent staining within the mesangium as 1+ negative and no staining, and 2+ and 3+ positive intensity staining (<2+ and ≥2+). Evaluation was also made according to the Oxford MEST-C classification. The primary endpoint was the development of end-stage renal failure (ESRF), and kidney transplantation, and an increase of 30% in glomerular filtration rate (GFR) compared to the basal value, or an elevation in proteinuria to a nephrotic level (3.5 gr/day) were accepted as poor prognosis. Results Mesangial C3 deposition was determined in 603 (53.1%) patients. In the evaluation of basal values between the groups with and without deposition, no statistically significant difference was determined in respect of age, gender, BMI, proteinuria level, or the presence of hypertension. In the follow-up period of mean 78 months survival, no significant difference was determined between the two groups in respect of the primary endpoint (C3+:53.1% vs. C3-:46.9%, p = 0.43). A significant correlation was determined between C3 deposition and segmental glomerulosclerosis (S1) according to the Oxford MEST-C classification (p = 0.001). Conclusion Although a correlation was seen between mesangial C3 deposition and the S1 MEST-C classification, the use of these alone or together as a prognostic factor in IgAN is not appropriate.

Use of angiotensin converting enzyme inhibitors in chronic kidney disease - a review of the literature

Introduction: Chronic Kidney Disease (CKD) has become one of the most common chronic diseases of the XXI century and affects around 16% of the world's population. Despite the advancements of contemporary science and a range of therapeutic methods it considered a progressive and irreversible process. Nevertheless, use of ACEI halts the progression of the disease and postpones the necessity of renal replacement therapy and is the method of choice for this group of patients. 
 Purpose of the work: The article reviews current literature and writing regarding Chronic Kidney Disease (CKD) and the impact of ACEI on the progression of this condition. 
 Materials and methods: The sources available in the PubMed database have been analyzed using the keywords: “ACEI”, “angiotensin-converting-enzyme inhibitors”, ”chronic kidney disease”, “CKD”. Related publications to the topic of the work have been selected and utilized. 
 Description of the state of knowledge: Pharmacological therapy using ACEI is the main method of treatment for patients with CKD and should primarily serve to reduce proteinuria and control blood pressure. It inhibits the progression of the disease and delays the development of end-stage renal failure. However, the treatment of CKD using ACEI is controversial in cases of advanced stages of the disease. 
 Summary: ACEI inhibitors are one of the major advances in the treatment of patients dealing with CKD. Due to the increasing number of cases of the disease being observed, further research will be needed regarding the use of these drugs. Particularly ambiguous is the therapy for patients with advanced, just before end-stage renal failure, which will require a more in-depth analysis of these cases.

Interpretation of Urine Routine Report of a Diabetic Patient

Introduction: Diabetic patients are at an increased risk of multiple complications, among which one of the most dreaded complications is diabetic nephropathy. Early diagnosis and appropriate management will at least prolong the life of the kidney and prevent the development of end-stage renal failure. Materials and Methods: Simple urinalysis is a useful tool for early diagnosis of diabetic kidney disease and helps differentiate between diabetic and nondiabetic kidney diseases. In this review, we have discussed the usefulness of urinalysis for a diabetic patient. Results: Early detection of an abnormality can be an alarming sign, and we can diagnose treatable causes of renal failure in diabetic patients. Conclusions: History, examination, and urinalysis are sufficient in most of the cases for diagnosing diabetic kidney disease. Renal biopsy is indicated in special situations where diagnosis cannot be made even after appropriate non-invasive investigations. Few limitations of the study are resource settings and knowledge of this simple test to predict an alarming sign of the kidney disease.

POS-191 PREDICTORS OF THE DEVELOPMENT AND OUTCOME OF KIDNEY DAMAGE IN CHILDREN WITH TYPE 1 DIABETES MELLITUS

The leading place among the specific complications of type 1 diabetes mellitus (DM 1) is occupied by kidney damage, leading to a decrease in the quality of life, where the inevitable outcome is the development of end-stage renal failure.

ХАРАКТЕРИСТИКА γδТ-ЛИМФОЦИТОВ У ПАЦИЕНТОВ С IgA-НЕФРОПАТИЕЙ

Currently, IgA-nephropathy is the most common form of primary glomerulonephritis resulted in the development of end-stage renal failure, the causes of which are not only genetic, but also environmental factors that contribute to epigenetic changes in the both cellular and humoral immunity. The main triggers of chronic autoimmune inflammation in IgA-ne- phropathy are environmental factors such as industrial pollutants, infectious agents, allergens and nephrotoxic xenobiotics resulted in not only the disruption of immunoglobulin A production in mucosae but also changes in the composition of microbiota and mucosal lymphoid cells, including the minor population of γδT-lymphocytes. In this study, the composition of γδT-cells subsets, their activation potential and cytotoxic activity were determined as well as the correlation of γδT-cells immunophenotype with biochemical and histological parameters of disease progression were established in patients with IgA-nephropathy. The redistribution of γδT-lymphocytes subsets in peripheral blood of patients with IgA-nephropathy was found characterizing by a predominance of tissue-resident cells (Vδ1+ and Vδ3+T-lymphocytes) and a statistically significant decrease of Vδ2+T-cells subpopulation as compared to the control group. It was shown that γδT-lym- phocytes did not demonstrate the cytotoxic activity, however, the detected increase of activated marker HLA-DR expression on Vδ1+ and Vδ3+T-lymphocytes indicated their possible antigen-presenting role in disease pathogenesis. The obtained results can be used as potential biomarkers in the early diagnosis of autoimmune kidney pathology.

ПЕРВЫЙ ОПЫТ ИСПОЛЬЗОВАНИЯ БИОАНАЛОГА ОРИГИНАЛЬНОГО ПРЕПАРАТА ЭКУЛИЗУМАБА ДЛЯ ПРОФИЛАКТИКИ ВОЗВРАТА АТИПИЧНОГО ГЕМОЛИТИКО-УРЕМИЧЕСКОГО СИНДРОМА В ПОЧЕЧНЫЙ ТРАНСПЛАНТАТ У РЕБЕНКА

The article presents a clinical case of atypical hemolytic uremic syndrome (аHUS), the debut of which proceeded under the guise of a typical HUS. After 4 months of hemodialysis, the child did not need renal replacement therapy for the next 9 months. The development of end-stage renal failure required a molecular genetic study to clarify the diagnosis. The child has mutations in the genes of the complement regulatory proteins – factor I and MCP. The risk of aHUS recurrence with these genes mutations to a renal transplant without pathogenetic prophylaxis is up to 80%. The use of the Russian biosimilar eculizumab before and after kidney transplantation allowed to prevent the activation of complement and disease recurrence to transplanted organ.

Experience of application of rituximab with resistant focal-segmental glomerulosclerosis in adults: a series of observations and a brief review of literature

Steroid-resistant focal-segmental glomerulosclerosis (FSGS) with nephrotic syndrome (NS) is a progressive kidney disease with the rapid development of end-stage renal failure (ESRD). In recent years, attempts have been made to treat steroidresistant FSHS with anti-CD20 monoclonal antibodies, rituximab. Currently, only a few clinical case reports and series with contradictory results have been published. THE AIM of our study was to evaluate the effect of rituximab in patients with resistant to the therapy focal segmental glomerulosclerosis. MATERIALS AND METHODS : The study included 6 patients with confirmed diagnosis of FSGS. The inclusion criteria were the presence of steroid-resistant NS or to the other treatment regimens, including cyclosporin A, tacrolimus, mycophenolate mofetil, cyclophosphamide, and exclusion criteria were the secondary form of the disease. Patients were treated with one course of rituximab – 2 to 4 infusions (the total dose was 1.0–2.0 g). Laboratory parameters (daily proteinuria, albumin and eGFR CKD-EPI) were analyzed before rituximab, as well as 6 and 12 months after treatment. RESULTS : A partial remission of FSGS was achieved in one patient, stable renal function was maintained for 12 months follow-up. In 4 out of 6 patients, progression of the disease was observed with the development of ESRD in the period from 1 to 3 years, despite a decrease in the severity of NS. In one patient, the NS of the same severity persisted for 6 months after the treatment; no positive dynamics in proteinuria or serum proteins were observed. CONCLUSION : Thus, we did not show a significant effect of rituximab in patients with steroid-resistant FSGS. However, according to the literature the effect of rituximab has been achieved in approximately half of steroid-resistant FSGS cases, therefore further prospective clinical trials are needed.

Kidney disease screening among a low-income group of hospital staffs who have less opportunity

Background: The prevalence of chronic kidney disease (CKD) has been rapidly increasing worldwide, and its early screening is vital to prevent the development of end-stage renal failure. Population-based studies on detection at early stage of kidney disease and its prevalence are scanty in our country. Hence, taking advantage of the observance of the World Kidney Day 2019, we conducted a screening program for kidney disease organized at the Chattagram Maa-O-Shishu Hospital premises among a low-income group of hospital staffs. Methods: This was a cross-sectional observational study among a low-income group of hospital staffs, working at our hospital. Age, body weight, height, body mass index (BMI), and blood pressure were documented, and urinary protein and serum creatinine were measured at a single sitting. Kidney function was estimated by calculating the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease formula. Kidney function was classified according to the estimated GFR (eGFR) and Kidney Disease Outcomes Quality Initiative guidelines. Results: A total of 101 hospital staffs were studied. Majority of the participants (38%) were in the age group of 30–39 years. Among all, 24% of the participants had proteinuria (trace to ≥1 plus). The distribution of eGFR was symmetrical, with the majority (79%) of participants in the 60–89 ml/min category, 6.9% in the 30–59 ml/min category, and only 13.9% of the study population had eGFR >90 ml/min. An inverse relation between eGFR and age and a direct relation between eGFR and BMI were observed. Conclusion: Proteinuria, low GFR levels, and consequently the possibility of high burden of CKD are prevailing in the studied participants, and further targeted population-based studies are warranted to clarify these issues.

SAT-299 CD38 INHIBITION DECREASE RENAL OXIDATIVE STRESS IN DIABETIC KIDNEY DISEASE BY RESTORING OF SIRT3 ACTIVATION.

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease worldwide. Aging is recognized as one of the risk factors for the development of end-stage renal failure due to chronic kidney disease including DKD. Therefore, investigation of aging-related mechanisms would be needed to discover a novel therapeutic target to treat DKD. Nicotinamide adenine dinucleotide (NAD) levels decrease during aging and are involved in age-related metabolic decline. Previous report demonstrated that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of sirt3 activity. We already discovered that the expression of CD38 was significantly increased in diabetic kidney and reduction in Sirt3 activity contributes to mitochondrial oxidative stress by decreasing the activation of anti-oxidative enzymes in the kidney of diabetic model rats. So, we investigated whether the inhibition of CD38 suppress mitochondrial oxidative stress through restoring of Sirt3 activity in diabetic rats and high glucose-incubated human renal tubular epithelial cells (HK2 cells). We used Male non-diabetic Zucker Lean (ZL) and type2 diabetes model rats, Zucker Diabetic Fatty rats (ZDFRs). CD38 inhibitor, apigenin or saline were prepared for oral gavage at 20mg/kg/day for 5 times by a week ,continued 4weeks and sacrificed at 28 weeks of age. In vitro study, HK2 cells were cultured in standard or high glucose condition and were treated for 48 hours with 10 μM apigenin or DMSO. At 28 weeks of age, compared to ZL, ZDFRs exhibited elevated HbA1c levels, heavier kidney weight, increased urinary albumin, liver type fatty acid binding protein (L-FABP), and 8-hydroxy-2’ -deoxyguanosine (8-OHdG), excretion, histological tubulo-interstitial fibrosis. In the immunostaining, increased CD38 positive cell in the kidney, particularly tubulo-interstitial area. Expression of mRNA and protein of CD38 were all significantly elevated in renal cortex. Administration of apigenin inhibited mRNA and protein expression of CD38, decreased albumin/L-FABP/8-OHdG excretion and ameliorated tubulo-interstitial fibrosis. Apigenin suppressed overexpression of CD38 in diabetic kidney and may ameliorated tubular cell damage. In addition, ZDFRs showed abnormal mitochondrial morphology, such as swelling and loss of cristae in primal tubular cell. In renal mitochondria, the NAD+/NADH ratio was reduced, and acetylation levels of mitochondrial antioxidant enzymes such as isocitrate dehydrogenase 2 (IDH2) and superoxide dismutase (SOD2), regulated by sirt3 were increased in ZDFRs. While apigenin restored abnormal mitochondrial morphology, increased NAD+/NADH ratio and reduced the acetylation of IDH2 and SOD2. Similarly, high glucose medium incubation in HK2 cell elevated CD38 levels associated with the reduction in NAD+/NADH ratio and increasing acetylation levels of SOD2 and IDH2. Administration of apigenin increased NAD+/NADH ratio, decreased SOD2 and IDH2 acetylation. Administration of the CD38 inhibitor, apigenin restored the NAD+/NADH ratio, decreased the levels of IDH2 and SOD2 acetylation and renal oxidative stress. Therefore, inhibition of CD38 may be a therapeutic target for the suppression of DKD.

Gasless laparoscopic nephrectomy in patients with autosomal dominant polycystic kidney disease

Introduction. Autosomal dominant polycystic kidney disease (PKD) is one of the most common hereditary diseases leading to the development of end-stage renal failure. According to modern concepts, nephrectomy of polycystic-altered kidneys in such patients is performed in the event of complications, as well as in order to prepare for kidney transplantation. The creation of intense carboxyperitoneum leads to carbon dioxide resorption and the development of hypercapnia and respiratory acidosis in the patient. Taking into account the age of patients and the high incidence of cardiovascular and valvular pathology in patients with PKD, this fact becomes significant and can lead to the development of severe complications. The solution to this problem, in our opinion, is to perform laparoscopic nephrectomy under low-pressure carboxyperitoneum (LPC).
 Materials and methods. In the period from 2013 to 2018, 55 monolateral laparoscopic nephrectomies were performed in 36 patients with PKD. The study identified 2 groups of patients. The study group included 8 patients who were diagnosed at the preoperative stage with cardiovascular disease performed LPC (12 operations). The second group was represented by 28 patients who were operated laparoscopically with the creation of intense carboxyperitoneum (41 operations). Workspace when LPC was created with the help of laparolift – mechanical device for lifting the abdominal wall on the abdominal cavity.
 Results. The mean duration of surgery in the groups was 126 ± 18 and 114 ± 11 minutes, respectively (p < 0.05). Intraoperative blood loss was significantly different: in the comparison group – 225 ± 45 ml, in the study group – 440 ± 76 ml (p < 0.05). Mean blood pCO2 and pH levels in the study group were 38.2 ± 2.7 mm Hg and 7.371 ± 0.021, the comparison group – 44.4 ± 3.8 mm Hg and 7.231 ± 0.035 (p < 0,05). Among the patients who underwent LPC, there was one fatal outcome. The frequency of postoperative complications was 16.6% (2) in the study group and 12.2% (5) in the comparison group.
 Summary. Laparoscopic nephrectomy in conditions of low pressure carboxyperitoneum allows to completely avoid the development of hypercapnia and respiratory acidosis in the patient, to prevent severe cardiovascular complications despite the high risk of their development among patients with PKD.

An Unusual Presentation of a Child with Hyperoxaluria

Introduction: Hyperoxaluria is a common abnormal finding in patients with nephrolithiasis, especially in children in contrary to adults. Overall, it is a rare disorder with the four main types of primary, enteric, dietary and idiopathic. The disorder is characterized by overproduction of oxalate that leads to nephrocalcinosis and eventual development of end-stage renal failure. Case Presentation: We report the case of a 2-year-old boy presented with multiple episodes of seizure, gastrointestinal bleeding, loss of consciousness and rise in blood urea nitrogen (BUN) and creatinine (Cr). He underwent imaging study and lumbar puncture with the suspicion of encephalitis. With more history-taking, we understood that he was previously under treatment for nephrocalcinosis. Finally, he underwent dialysis and the level of consciousness improved. His diagnosis was confirmed by renal biopsy and establishing the existence of extensive tubular and interstitial crystal deposition in his kidneys. Conclusions: The case illustrates the need for the early diagnosis of this disorder to prevent systemic oxalosis that affects many organs resulting in severe morbidity and mortality and raising the suspicion of primary hyperoxaluria in childhood progressive renal failure with massive nephrocalcinosis, especially if accompanied by a positive family history. In these cases, complications should be explained to increase drug compliance.

Renal Mitochondrial Oxidative Stress Induced by NAD+-Dependent Sirt3 Inactivation via Overexpression of CD38 (NAD+ase) in Diabetic Kidney Disease

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease worldwide. Although the detailed pathogenesis of DKD is not elucidated yet, aging is recognized as one of the risk factors for the development of end-stage renal failure due to chronic kidney disease including DKD. Therefore, investigation of aging-related mechanism would be a novel therapeutic target for DKD. NAD levels decrease during aging. Previous report demonstrated that expression and activity of the CD38 (NADase) increased with aging, and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of Sirt3 activity. However, the role of CD38 in the pathogenesis for DKD has never been investigated. In this study, we evaluated the role of CD38 on the mechanisms of renal mitochondrial oxidative stress which is related to changing Sirt3 activity, in Zucker Diabetic Fatty rats (ZDFRs) and in cultured HK2 cells under high-glucose condition. At 28 weeks of age, the ZDFRs exhibited elevated HbA1c levels, heavier kidney weight, increased urinary albumin, L-FABP and 8-OHdG excretion, histological tubulo-interstitial fibrosis and tubular cell damage, compared to nondiabetic Zucker Lean rats. Additionally, in renal mitochondria, the NAD+/NADH ratio was reduced, and acetylation levels of mitochondrial antioxidant enzymes, IDH2 and SOD2, which are regulated by Sirt3, were increased in ZDFRs. Similarly, in cultured HK2 cells under high-glucose condition, CD38 expression was increased, resulting in the reduction of NAD+/NADH ratio and Sirt3 activity, which increased in acetylation levels of IDH2 and SOD2. Administration of the CD38 inhibitor, apigenin, to ZDFRs and HK2 cells, restored the NAD+/NADH ratio, decreased the levels of IDH2 and SOD2 acetylation. Therefore, restoring Sirt3 activation by suppression of CD38 may be a novel therapeutic target for DKD. Disclosure Y. Ogura: None. M. Kitada: Research Support; Self; Astellas Pharma US, Inc., Kyowa Hakko Kirin Co., Ltd., Daiichi Sankyo Company, Limited, Ono Pharmaceutical Co., Ltd., Novartis Pharma K.K., Sumitomo Dainippon Pharma Co., Ltd., Boehringer Ingelheim GmbH, Taisho Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Corporation. I. Monno: None. A. Watanabe: None. D. Koya: None.

Membranous nephropathy: a retrospective observational study of membranous nephropathy in north east and central London

BackgroundMembranous nephropathy (MN) is the leading cause of nephrotic syndrome in adults. MN is a clinically heterogeneous disease and it is difficult to accurately predict outcomes (including end stage renal failure) at presentation and whom to treat with potentially toxic therapies. We aimed to identify factors predicting outcome in MN in our cohort from two large tertiary London units by undertaking a retrospective data analysis of 148 biopsy-proven MN patients from North East and Central London between 1995 and 2015.MethodsReview of clinical and biochemistry databases.ResultsSurprisingly, patients that reached end stage renal failure (ESRF) had a less severe nephrosis compared to those that did not develop ESRF; serum albumin 33 g/L (3.3 g/dL) versus 24 g/L (2.4 g/dL), p = 0.002 and urinary protein creatinine ratio (uPCR) 550 mg/mmol (5500 mg/g) versus 902 mg/mmol (9020 mg/g), p = 0.0124. The correlation with ESRF was strongest with the presenting creatinine; 215 μmol/L (2.43 mg/dL) compared to 81 μmol/L (0.92 mg/dL), p < 0.0001. Patients presenting with creatinine of >120 μmol/L (1.36 mg/dL; corresponding to an eGFR of ≤60 ml/min in non-Black males) had an increased rate of ESRF and a faster decline. Other traditional risk factors for progression were not significantly associated with ESRF.Black patients presented with higher serum creatinine but no statistically significant difference in the estimated glomerular filtration rate, a higher rate of progression to ESRF and had a poorer response to treatment.ConclusionsThis ethnically diverse cohort does not demonstrate the traditional risk profile associated with development of ESRF. Thus, careful consideration of therapeutic options is crucial, as current risk modelling cannot accurately predict the risk of ESRF. Further studies are required to elucidate the role of antibodies and risk genes.

Anti-gbm Rapidly Progressive Glomerulonephritis (Syndroma Goodpasture): A Case Report

Abstract Goodpasture syndrome is a severe illness caused by the formation of antibodies to the glomerular basement membrane and alveolus with consequential damage to renal and pulmonary function. With current therapy, long-term survival is more than 50%. Before, the mortality was higher than 90%. In our patient, the disease began as dysuria, continued as anaemic syndrome, and ended with the development of end-stage renal failure. Immunosuppressive therapy with pulse doses of methylprednisolone and cyclophosphamide has put the disease into remission, but the permanent impairment of renal function remained. Early diagnosis of Goodpasture syndrome helps preserve renal function and improves patients’ survival. In patients who achieve remission, a kidney transplant can be considered. Currently, our patient is awaiting transplantation

Anti-GBM rapidly progressive glomerulonephritis (Syndroma Goodpasture): A case report

Goodpasture syndrome is a severe illness caused by the formation of antibodies to the glomerular basement membrane and alveolus with consequential damage to renal and pulmonary function. With current therapy, long-term survival is more than 50%. Before, the mortality was higher than 90%. In our patient, the disease began as dysuria, continued as anaemic syndrome, and ended with the development of end-stage renal failure. Immunosuppressive therapy with pulse doses of methylprednisolone and cyclophosphamide has put the disease into remission, but the permanent impairment of renal function remained. Early diagnosis of Goodpasture syndrome helps preserve renal function and improves patients’ survival. In patients who achieve remission, a kidney transplant can be considered. Currently, our patient is awaiting transplantation

Screening for chronic kidney diseases among an adult population

Chronic kidney disease (CKD) is now one of the major health problems all over the world and its early screening is vital to prevent the development of end-stage renal failure. This study was designed to evaluate the proportion of urban adults suffering from CKD as well as to have a preliminary idea about the determinants of this disorder. The screening program for CKD was arranged in a public place in Dhaka city, Bangladesh, and involved 634 adult participants (>18 years of age) selected on first-come first-served basis. Socio-demographic, anthropometric, and clinical data were collected. Urinary protein was tested by the dipstick method, and serum glucose and creatinine were measured by an auto-analyzer. Estimated glomerular filtrate rate (eGFR) was calculated by using standard formula. CKD was diagnosed and classified according to the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines. A total of 12.8% of the subjects were found to have CKD of whom 2.7% were in Stage 1, 4.1% in Stage 2, and 6% were in Stage 3. The proportion was strongly influenced by age, with the highest prevalence (38.5%) found at 60 years and above. The CKD group showed higher body mass index, waist-hip ratio, and systolic blood pressure, compared with their non-CKD counterparts (P = 0.02). On multiple regression analysis (after adjustment of some confounding variables), age, random blood sugar, and education showed significant association with the development of CKD. A substantial number of urban adults in Dhaka were found to be unaware about the existence of CKD and large-scale prevention programs should be undertaken to reduce the classical risk factors of these disorders.

Management of Hyperglycemia in Hospitalized Patients with Renal Insufficiency or Steroid-Induced Diabetes

Pharmacologic doses of glucocorticoids and chronic renal failure are challenging comorbidities and complications for safe and effective dosing of insulin for the management of hospitalized patients with diabetes. Glucocorticoids are used widely in hospitalized patients and will commonly provoke new-onset hyperglycemia in patients without a prior history of diabetes or will provoke severely uncontrolled hyperglycemia in patients with known diabetes. Insulin therapy is invariably necessary for the treatment of glucocorticoid-induced hyperglycemia and must be tailored to the pharmacodynamics of the glucocorticoid being given. Renal failure causes a decrease in the clearance of insulin, especially exogenous injected insulin. Dosing algorithms for hospitalized patients should be adjusted for patients with renal failure in order to minimize hypoglycemia. Many patients with type 2 diabetes will need little or no therapy after the development of end-stage renal failure. Care must be taken to avoid the overtreatment of hyperglycemia.