Appearance Of Microalbuminuria Research Articles

Microalbuminuria in Rats Treated with D-Nitroarginine Methyl Ether.

Microalbuminuria is an early symptom and prognostic marker of the progression of renal pathology. The analysis of the role of anionic components of the renal glomeruli in the albumin retention and the development of a model of minimal changes in the glomerular filter leading to the appearance of microalbuminuria are relevant. The effect of organic cations D-arginine methyl esters (D-AME) and D-nitroarginine (D-NAME) on the excretion of albumin by the kidneys in rats was studied. D-AME had no effect on urinary albumin excretion in rats. D-NAME caused microalbuminuria, which persisted for more than a day and sharply increased after injection of vasopressin. The number of anionic sites labeled with polyethyleneimine decreased in the structures of the glomerular filter. D-NAME-induced microalbuminuria can later serve as a model for studying nephroprotective or damaging factors.

Heart failure correction in patients with chronic renocardiac syndrome

Abstract Funding Acknowledgements Type of funding sources: None. In case of inadequate diagnosis and correction of the basic disease, which triggers the development of chronic heart failure (CHF), left ventricular (LV) remodeling leads to myocardial dysfunction and decompensation. Patients who entered the study EUCLID, demonstrated nephroprotective effect of lisinopril, which reduces the appearance of microalbuminuria. Target Study the effectiveness of lisinopril in the correction of CHF in patients with chronic renocardiac syndrome based on a study of LV diastolic function. Methods 59 patients with chronic renocardiac syndrome were investigated. All patients received lisinopril 10-20 mg per day. LV diastolic function was evaluated for Acuson Sequoia-512 before and after treatment. Results Changes in the kinetics of myocardial contractility were characterized by high amplitude of the interventricular septum, increased by 20%, end-systolic contractility index by 9.1%, the degree of shortening of the left ventricular size by 11.4%. A significant decrease in the rate of diastolic filling by passive relaxation (E) of 23.4% and a filling rate due to atrial contraction (A) at 20%. Violation of intracardiac hemodynamics as manifested by increasing the restrictive properties of the myocardium, as well as reducing the effectiveness of time and deceleration rate of early LV filling flow by 23.2 and 27.4%, increase and decrease of LV filling time active by reducing atrial 49.9% . Decreased as the time of isovolumic LV relaxation of the heart. During treatment with lisinopril was an increase in ejection fraction (EF) of 16.4% (p=0.004) or 53.2% (49.1, 58.9) to 61.9% (53.4, 68.0 ). The rate of mitral filling period of relaxation (Ve) increased from 0.53 m/s (0.43, 0.58) to 0.56 m/s (90.47, 0.63), or 5.7 % (p=0.039), while maintaining the diastolic filling due to atrial contraction. This has led to the restructuring of diastolic filling of the normal type, which was confirmed by the change of the reflectance upwards: Ratio of Ve/Va to treatment was 1.45 units. (1.02, 1.63), vand during treatment - 1.58 units (1.21, 1.90), or a 9.0% increase (p = 0.013). Equally, there was a decrease IVRT: from 61.9 ms (54.6, 78.8) to 56.4 ms (50.3, 72.4) or 8.9% (p=0.044). Conclusions Improvement of LV diastolic function is due to improved myocardial relaxation. ACE inhibitor (lisinopril), as a means of LV remodeling, reduce the degree of diastolic dysfunction by improving myocardial relaxation in patients with chronic renocardiac syndrome.

Urinary Proteome Differences in Canine Diabetes with and without the Presence of Microalbuminuria.

Simple SummaryCanine diabetes is a serious disease, which can lead to numerous complications. There are limited data on urine proteomics in dogs, and none of the effect of diabetes mellitus on the urine proteome. In this study we aimed to analyze the protein composition of the urine collected from the healthy animals and compare it with two diabetic groups (normoalbuminuric and microalbuminuric). There are significant differences between these three groups, and we believe that the identified proteins hold promise as a potential diagnostic tool, which can be later on used in clinical practice, and for better understanding of the disease.In this study we aimed to analyze the protein composition of the urine collected from the healthy animals and compare it to the two diabetic groups (DM I normoalbuminuric diabetic dogs; DM II diabetic dogs with microalbuminuria). We tried to identify potential urinary proteins which could be up- or downregulated in diabetic patients even before the appearance of microalbuminuria. Methods: After obtaining urine, we performed two-dimensional electrophoresis, followed by Delta2D software analysis, which allowed for selection and identification with MALDI-TOF spectrometry, statistically significant differentially expressed proteins. Our study revealed 286 common protein spots on 2D gels from the diabetic and control group. From these proteins five were positively identified by MALDI-TOF MS. To further evaluate the five differentiating proteins, the Panther program was used to assign them to appropriate biological process. Conclusion: Significant number of identified proteins play a role in intracellular signaling—vesicle formation, bonding, transport through membranes. This may suggest that first signs of kidney diabetic cellular impairment may be seen in the urine composition before any clinical signs occur.

ADVANCE research 20 years later

Observational and interventional studies have shown that intensive blood pressure control may benefit in patients with diabetes. The Action in Diabetes and Vascular Disease: Preterax and Diarnicron MR Controlled Evaluation (ADVANCE) international randomized, controlled, clinical trial was launched in 2001. According to the results of the study, the risk of major micro- and macrovascular events (primary endpoint) significantly decreased by 9%, while the risks of cardiovascular death and death from any cause decreased by 18% and 14%, respectively. There was a decrease in the risks of microvascular complications – any renal event, the appearance or worsening of nephropathy and the appearance of microalbuminuria by 21%, 18% and 21%, respectively. The results of the antihypertensive part of the ADVANCE study supplemented the expanding evidence base and served as the basis for changing clinical guidelines for the management of patients with hypertension and diabetes. According to the updated joint guidelines of the European Society of Cardiology / European Association for the Study of Diabetes (ESC/EASD), the target systolic / diastolic blood pressure levels should be 130/80 mmHg, with some exceptions, and the fixed combination of the RAAS blocker with a diuretic or calcium antagonist is suggested as first-line therapy.The observational ADVANCE-ON study, which enrolled 8494 patients out of 11 140 patients randomized to the ADVANCE study, found a memory effect, or ‘inheritance’, in which intensive blood pressure control during the study had a beneficial effect on various outcomes after its termination. These findings highlight the importance of achieving and maintaining optimal blood pressure control to reduce the risk of micro- and macrovascular complications.

Association of neutrophil-gelatinase-associated lipocalin with microvascular complications in patients with type 2 diabetes: a cross-sectional study

Eighty-two patients with type 2 diabetes were enrolled in our study. Urinary microalbumine and NGAL levels were measured in urine samples over 24 hours. We also studied NGAL levels in serum. All patients went through an ophthalmologic examination. The results were evaluated based on the presence of microalbuminuria and retinopathy. There were no significant differences in serum and urine NGAL levels between normoalbuminuric (n = 66) and microalbuminuric (n = 16) patients. We also did not find any significant difference in patients with retinopathy (n = 16) or without retinopathy (n = 66). There are controversial findings about the role of NGAL in diabetic patients in medical literature. Standard values of urine and serum NGAL levels have yet to be determined. Our study suggests that NGAL is not a useful marker to differentiate microalbuminuric patients from normoalbuminuric subjects. We also did not find a relationship between NGAL levels and the presence of retinopathy. Additional studies with larger sample sizes will be required to confirm or refute these findings.

Urinary neutrophil gelatinase-associated lipocalin in type 2 diabetes: Relation to nephropathy and retinopathy

BackgroundDiabetes mellitus is the leading cause of end stage renal disease worldwide. Early identification of diabetic nephropathy even before appearance of microalbuminuria is a challenge for early prevention of occurrence and progression of this complication. Neutrophil gelatinase-associated lipocalin is a small protein that belongs to the lipocalin protein. Urinary neutrophil gelatinase-associated lipocalin is a promising early marker in different renal problems. Aim of the workTo measure urinary neutrophil gelatinase-associated lipocalin in type 2 diabetic patients and to assess its role as an early marker for diagnosis of diabetic nephropathy and diabetic retinopathy. Patient and methodsThe current study included 60 subjects with type 2 diabetes and 20 healthy control subjects. Diabetic subjects were divided into 3 groups according to urinary albumin creatinine ratio; 20 normoalbuminuric patients, 20 micro-albuminuric patients and 20 macroalbuminuric patients. They were subjected to history taking, full clinical examination, fundus examination, anthropometric measurement, urinary neutrophil gelatinase-associated lipocalin and urinary albumin creatinine ratio. ResultsUrinary neutrophil gelatinase-associated lipocalin was higher in all diabetic groups than in the control group, with no difference in between diabetic groups. The difference was of great value when comparing normoalbuminuric group with control as albumin creatinine ratio was not different while the urinary neutrophil gelatinase-associated lipocalin was statistically significant (5.94 ± 1.85 ng/dl vs 1.96 ± 0.65, p < 0.001). No correlation was found with retinopathy. ConclusionUrinary neutrophil gelatinase-associated lipocalin is a sensitive marker for early detection of diabetic nephropathy even in normoalbuminuric patients denoting early tubular damage before microalbuminuria. It is not correlated with retinopathy.

Urinary Vitamin-D Binding Protein as an Early Predictor of Diabetic Nephropathyin Type 1 and Type 2 Diabetes

Diabetic nephropathy (DN) is the most common microvascular complication that may lead to chronic renal failure in diabetic patients. Till now microalbuminuria, with its restrictions, is the early marker of DN, appeared after the disease exacerbation. Thus, new biomarkers are required to predict the early onset of DN before the appearance of microalbuminuria. The aim of this study is to investigate the possible use of uVDBP in the early prediction of DN. Fifty diabetic patients with DN and 40 diabetic patients without DN for both types of diabetes were enrolled in this study. All patients were tested for uACR, uVDBP (measured by ELISA), and blood HbA1c. The results demonstrated a highly significant elevation of uACR, HbA1c and uVDBP in diabetic patients with DN compared to those without DN. uVDBP exhibited a strong positive correlation with HbA1c and uACR in DN patients. ROC curve analysis showed a greater AUC (0.93), and cutoff value was &gt;152 ng/ml with 94% sensitivity and 82% specificity for early detection of DN. These findings suggesting the sensitive and potential role of uVDBP in the early prediction and diagnosis of DN in type 1 and type 2 diabetes.

Losartan prevents the imbalance between renal dopaminergic and renin angiotensin systems induced by fructose overload. l-Dopa/dopamine index as new potential biomarker of renal dysfunction

BackgroundThe renin angiotensin system (RAS) and the renal dopaminergic system (RDS) act as autocrine and paracrine systems to regulate renal sodium management and inflammation and their alterations have been associated to hypertension and renal damage. Nearly 30–50% of hypertensive patients have insulin resistance (IR), with a strong correlation between hyperinsulinemia and microalbuminuria. ObjectiveThe aim of this study was to demonstrate the existence of an imbalance between RAS and RDS associated to IR, hypertension and kidney damage induced by fructose overload (FO), as well as to establish their prevention, by pharmacological inhibition of RAS with losartan. Materials/MethodsNinety-six male Sprague-Dawley rats were randomly divided into four groups and studied at 4, 8 and 12 weeks: control group (C4, C8 and C12; tap water to drink); fructose-overloaded group (F4, F8 and F12; 10% w/v fructose solution to drink); losartan-treated control (L) group (L4, L8 and L12; losartan 30 mg/kg/day, in drinking water); and fructose-overloaded plus losartan group (F + L4, F + L8 and F + L12, in fructose solution). ResultsFO induced metabolic and hemodynamic alterations as well as an imbalance between RAS and RDS, characterized by increased renal angiotensin II levels and AT1R overexpression, reduced urinary excretion of dopamine, increased excretion of l-dopa (increased l-dopa/dopamine index) and down-regulation of D1R and tubular dopamine transporters OCT-2, OCT-N1 and total OCTNs. This imbalance was accompanied by an overexpression of renal tubular Na+, K+-ATPase, pro-inflammatory (NF-kB, TNF-α, IL-6) and pro-fibrotic (TGF-β1 and collagen) markers and by renal damage (microalbuminuria and reduced nephrin expression). Losartan prevented the metabolic and hemodynamic alterations induced by FO from week 4. Increased urinary l-dopa/dopamine index and decreased D1R renal expression associated to FO were also prevented by losartan since week 4. The same pattern was observed for renal expression of OCTs/OCTNs, Na+, K+-ATPase, pro-inflammatory and pro-fibrotic markers from week 8. The appearance of microalbuminuria and reduced nephrin expression was prevented by losartan at week 12. ConclusionThe results of this study provide new insight regarding the mechanisms by which a pro-hypertensive and pro-inflammatory system, such as RAS, downregulates another anti-hypertensive and anti-inflammatory system such as RDS. Additionally, we propose the use of l-dopa/dopamine index as a biochemical marker of renal dysfunction in conditions characterized by sodium retention, IR and/or hypertension, and as a predictor of response to treatment and follow-up of these processes.

Exercise-induced albuminuria is related to metabolic syndrome.

Microalbuminuria (MA) is a known marker for endothelial dysfunction and future cardiovascular events. Exercise-induced albuminuria (EiA) may precede the appearance of MA. Associations between EiA and metabolic syndrome (MS) have not been assessed so far. Our aim was to investigate this association in a large sample of apparently healthy individuals with no baseline albuminuria. This was a cross-sectional study of 2,027 adults with no overt cardiovascular diseases who took part in a health survey program and had no baseline MA. Diagnosis of MS was based on harmonized criteria. All patients underwent an exercise test (Bruce protocol), and urinary albumin was measured before and after the examination. Urinary albumin-to-creatinine ratio (ACR) values before and after exercise were 0.40 (0.21-0.89) and 1.06 (0.43-2.69) mg/g for median (interquartile range) respectively. A total of 394 (20%) subjects had EiA; ACR rose from normal rest values (0.79 mg/g) to 52.28 mg/g after exercise (P < 0.001); this effect was not shown for the rest of the study population. EiA was related to higher prevalence of MS (13.8% vs. 27.1%, P < 0.001), higher metabolic equivalents (P < 0.001), higher baseline blood pressure (P < 0.001), and higher levels of fasting plasma glucose, triglycerides, and body mass index (P < 0.001). Multivariate binary logistic regression model showed that subjects with MS were 98% more likely to have EiA (95% confidence interval: 1.13-3.46, P = 0.016). In conclusion, EiA in the absence of baseline MA is independently related to MS.

Cystatin C - A Biomarker for Early Nephropathy in Type 2 Diabetic Patients

Diabetic nephropathy (DN) is a serious complication of diabetes associated with an increased risk of mortality, and cardiovascular and renal outcomes. Cystatin C, a 13 kD non-glycosylated basic protein, may be elevated in diabetic patients even before the appearance of microalbuminuria, and can be used as useful marker for detecting nephropathy in patients with normoalbuminuria (early nephropathy). We reviewed the recent literatures to determine if serum or urine cystatin C measurements could be useful as a marker to detect early DN in type 2 diabetic patients. Our search identified a total of 23 studies that have been published to date. Cystatin C measurement was carried out using immunoturbidimetric assays, Dade Behring Cystatin C assay, particle enhanced nephlometric immnuno assays, ELISA kits, or latex agglutination tests. Serum or urinary levels of cystatin C were elevated in type 2 diabetic patients compared to non-diabetic controls, including in patients who had no signs indicating nephropathy (without microalbuminuria). A significant positive correlation was found between cystatin C levels and albuminuria, suggesting its ability as a marker reflecting the degree of renal impairment in type 2 DN. Despite the promise of cystatin C as a biomarker, further large, multicenter prospective studies are still needed to confirm its clinical utility as a screening tool for early type 2 DN in every day practice.

Urinary biomarkers for early diabetic nephropathy in type 2 diabetic patients.

Diabetic nephropathy (DN) is a serious complication of diabetes associated with increased risk of mortality, and cardiovascular and renal outcomes. Diagnostic markers to detect DN at early stage are important as early intervention can slow loss of kidney function and improve patient outcomes. Urinary biomarkers may be elevated in diabetic patients even before the appearance of microalbuminuria, and can be used as useful marker for detecting nephropathy in patients with normoalbuminuria (early DN). We reviewed some new and important urinary biomarkers, such as: Neutrophil gelatinase associated lipocalin (NGAL), N-acetyl-beta-glucosaminidase (NAG), Cystatin C, alpha 1-microglobulin, immunoglobulin G or M, type IV collagen, nephrin, angiotensinogen and liver-type fatty acid–binding protein (L-FABP) associated with early DN in type 2 diabetic patients. Our search identified a total of 42 studies that have been published to date. Urinary levels of these biomarkers were elevated in type 2 diabetic patients compared with non-diabetic controls, including in patients who had no signs indicating nephropathy (without microalbuminuria), and showed positive correlation with albuminuria. Despite the promise of these new urinary biomarkers, further large, multicenter prospective studies are still needed to confirm their clinical utility as a screening tool for early type 2 DN in every day practice.

Efficacy of urinary N-acetyl-β-D-glucosaminidase to evaluate early renal tubular damage as a consequence of type 2 diabetes mellitus: a cross-sectional study

We assessed the prognostic accuracy of urinary N-acetyl-β-D-glucosaminidase (NAG), an early proximal tubular damage marker for the onset of diabetic nephropathy. The study included 491 eligible participants with 76 healthy controls, 194 type 2 diabetes mellitus (T2DM) patients with 0–5, 5–10, 10–15, and 15–20 years of T2DM duration, 71 microalbuminuric patients, 100 diabetic nephropathy patients, and 50 non-diabetic nephropathy patients. Fasting glucose, serum fructosamine, HbA1C, urinary microalbumin, serum creatinine, estimated glomerular filtration rate (eGFR), serum NAG, and urinary NAG were estimated. We compared urinary NAG activity with other well-established markers of diabetic nephropathy like microalbuminuria, eGFR, and serum creatinine. Urinary NAG excretion was increased by 8 and 12 folds in T2DM patients of 10–15 and 15–20 years of diabetes duration (p < 0.0001), respectively, without the appearance of microalbuminuria. The urinary NAG activity increased 16 and 18 fold in moderately increased albuminuria and diabetic nephropathy patients, respectively (p < 0.0001), without any change in non-diabetic nephropathy patients. A cutoff value of 3 U/L of urinary NAG has demonstrated a sensitivity of 96.1 % and a specificity of 100 % discriminating healthy controls from patients with T2DM duration of 10–15 years (AUC 1.000) and 15–20 years (AUC 0.999); microalbuminuria (AUC 0.999), and diabetic nephropathy (AUC 1.000). Urinary NAG excretion gradually increases with the increase in duration of diabetes and appeared much before the microalbuminuria, decreased eGFR, and increased serum creatinine. Thus, the urinary NAG may be considered as a potential site-specific early tubular damage marker leading to diabetic nephropathy.

Serum cystatin C and microalbuminuria in children with immune thrombocytopenia under short course of corticosteroids

BackgroundCorticosteroids are the universally accepted first line therapy for moderate and severe immune thrombocytopenia (ITP). ObjectivesWe investigated the effect of a short course prednisolone on serum cystatin C and the appearance of microalbuminuria as markers for renal injury in a group of ITP children. MethodsThe study involved 33 (19 males, 14 females) newly diagnosed ITP children divided into two groups; group I included 15 children with no or mild bleeding treated according to “watch and wait” policy; group II included 18 children of moderate or severe bleeding treated by oral prednisolone. Fifteen healthy, age and sex matched children were enrolled as a control group. Blood urea, serum creatinine, estimated glomerular filtration rate (eGFR) by Schwartz formula, serum cystatin C (by ELISA) and urinary albumin concentration (by immunoturbidimetric assay) were determined. ResultsThe baseline investigations were comparable in the three groups and were within the reference ranges. Corticosteroids of 12mg/kg cumulative dose had induced significant increments in serum creatinine [from 0.62±0.16 to 0.84±0.12mg/dL, p<0.0001] cystatin C [from 750.83±108.1 to 2300.55±991.94ng/ml, p<0.0001] and decreased eGFR [from 116.69±40.87 to 79.76±24.48ml/min/1.73m2, p=0.001] without change in urinary albumin concentration or induction of microalbuminuria in paired analysis. ConclusionAlthough not accompanied by microalbuminuria, steroid induced cystatin C elevation could be attributed in part to impaired GFR. Large population follow up studies are recommended to investigate the reversibility of this effect.

Obesidad y enfermedad renal crónica: Una peligrosa asociación

A higher frequency of chronic renal disease is observed in obese patients, suggesting a pathogenic association between both conditions. Obesity unmasks clinical manifestations of chronic kidney disease such as high blood pressure, which may accelerate its progression. Obesity also promotes hyper filtration and the appearance of microalbuminuria, activates the renin-angiotensin-aldosterone system and is associated with high levels of pro-inflammatory cytokines. Therefore weight reduction may slow the progression of chronic renal disease and reduce its associated cardiovascular risk factors.

Markers of and Risk Factors for the Development and Progression of Diabetic Kidney Disease

Diabetic kidney disease (DKD) occurs in 25%-40% of patients with diabetes. Given the dual problems of a significant risk of progression from DKD to end-stage renal disease (ESRD) and increased cardiovascular morbidity and mortality, it is important to identify patients at risk of DKD and ESRD and initiate protective renal and cardiovascular therapies. The importance of preventive therapy is emphasized further by worldwide increases in the incidence of diabetes. This review summarizes the evidence regarding the prognostic value and benefits of targeting established and novel risk markers for DKD development and progression. Family history of DKD, smoking history, and glycemic, blood pressure, and plasma lipid level control are established factors for identifying people at greatest risk of DKD development and progression. Absolute albumin excretion rate (AER) and glomerular filtration rate (GFR) measurements also are important, although AER categorization generally lacks the necessary specificity and sensitivity, and estimates of declining GFR are compromised by methodological limitations for GFRs in the normal-to-high range. Emerging risk markers for progressive loss of kidney function include markers of oxidation and inflammation, profibrotic cytokines, uric acid, advanced glycation end products, functional and structural markers of vascular dysfunction, kidney structural changes, and tubular biomarkers. Among these, the most promising are serum uric acid and soluble tumor necrosis factor receptor (type 1 and type 2) levels, especially in relation to GFR changes. At present, these can only be considered as risk markers because they only identify an individual at increased risk of progressive DKD and not necessarily related to the causal pathway promoting kidney damage. Further work is needed to establish whether modulating these factors improves the prognosis in DKD. Although change in urinary peptidome levels also is a promising marker, there currently is neither a clinical assay nor adequate studies defining its prognostic value. Until these or other novel markers become available for clinical use, predictive accuracy often may be increased with greater attention to established markers.

Vascular response to vasodilator treatment in microalbuminuric diabetic kidney disease.

Under common practice, the conventional diagnostic marker such as microalbuminuria determination does not recognized early stage of diabetic kidney disease (normoalbuminuria, chronic kidney disease stage 1, 2); due to the insensitiveness of the available marker. Treatment at later stage (microalbuminuria) simply slows the renal disease progression, but is rather difficult to restore the renal perfusion. Intrarenal hemodynamic study in these patients revealed an impaired renal perfusion and abnormally elevated renal arteriolar resistances. Treatment with vasodilators such as angiotensin converting enzyme inhibitor and angiotensin receptor blocker fails to correct the renal ischemia. Recent study on vascular homeostasis revealed a defective mechanism associated with an impaired nitric oxide production which would explain the therapeutic resistance to vasodilator treatment in microalbuminuric diabetic kidney disease. This study implies that the appropriate therapeutic strategy should be implemented at earlier stage before the appearance of microalbuminuria.

Urine albumin to creatinine ratio and echocardiographic left ventricular structure and function in patients with essential hypertension.

Appearance of microalbuminuria, particularly in patients with hypertension, might be associated with a higher prevalence of left ventricular (LV) dysfunction and geometric abnormalities. This study was undertaken to determine whether high urine albumin to creatinine ratio (UACR) as a sensitive marker for microalbuminuria can be associated with LV hypertrophy (LVH) and systolic and diastolic LV dysfunction. The study population consisted of 125 consecutive patients with essential uncomplicated hypertension. Urine albumin and creatinine concentration was determined by standard methods. LVH was defined as a LV mass index >100 g/m2 of body surface area in women and >130 g/m2 in men. Echocardiographic LV systolic and diastolic parameters were measured. The prevalence of microalbuminuria in patients with essential hypertension was 5.6 %. UACR was significantly no different in patients with LVH than in patients with normal LV geometry (21.26 ± 31.55 versus 17.80 ± 24.52 mg/mmol). No significant correlation was found between UACR measurement and systolic and diastolic function parameters, including early to late diastolic peak velocity (E/A) ratio (R=-0.192, p=0.038), early diastolic peak velocity to early mitral annulus velocity (E/E') ratio (R=-0.025, p=0.794), LV ejection fraction (R=0.008, p=0.929), and LV mass (R=-0.132, p=0.154). According to the receiver operator characteristic (ROC) curve analysis, UACR measurement was not an acceptable indicator of LVH with areas under the ROC curves 0.514 (95 % confidence interval 0.394-0.634). The optimal cut-off value for UACR for predicting LVH was identified at 9.4, yielding a sensitivity of 51.6 % and a specificity of 48.3 %. In patients with uncomplicated essential hypertension, abnormal systolic and diastolic LV function and geometry cannot be effectively predicted by the appearance of microalbuminuria.

Urinary κ and λ immunoglobulin light chains in normoalbuminuric type 2 diabetes mellitus patients

Kidney disease is one of the major chronic microvascular complications of diabetes. Tubular involvement may precede glomerular involvement and the appearance of microalbuminuria. The aim of the study was to evaluate quantitatively immunoglobulin light chains (IgLCs), kappa and lambda excretion in the urine of patients with type 2 diabetes mellitus with normoalbuminuria and with microalbuminuria compared to control group. Urinary IgLCs levels of the control group were significantly lower than diabetic patients with normoalbuminuria and diabetic patients with albuminuria. IgLCs were significantly associated with the duration of disease and negatively with estimated glomerular filtration rate. Type 2 diabetic patients can have significantly raised concentrations of urinary IgLCs before microalbuminuria or renal disease occurs. Further investigations are recommended to assess LC evaluation in the early management of diabetic renal disease.

Early histological changes in the kidney of people with morbid obesity

Morbid obesity represents a major health problem with increasing incidence worldwide. The clinical manifestation of renal involvement in obesity is proteinuria, and the histological feature is glomerulomegaly with or without focal and segmental glomerulosclerosis (FSGS). In this study, we have investigated the very early histological changes in kidneys of people with morbid obesity and no proteinuria. Patients and methods. Eighteen patients with body mass index (BMI) >50 kg/m(2) who underwent a variant of biliopancreatic diversion with Roux-en-Y reconstruction (BPD-RYGBP) and consented to undergo a renal biopsy during the surgical procedure were included in the study. The estimation of early histological changes was performed on light (n = 18) and electron microscopy (n = 13). The mean glomerular cross-sectional area was 30 943 +/- 10,984 microm(2) that is higher than that observed in non-obese individuals. In 21% of the examined glomeruli, the glomerular planar surface area (GPSA) was >40,000 microm(2). Thickening of the glomerular basement membrane (GBM) and scattered paramesangial deposits were identified in 9 of 13 patients (70%) whose renal tissue was examined by electron microscopy. A reduction in the slit pore frequency was observed in obese patients due to extensive foot process effacement. Significant positive correlations between mean GPSA and body weight (r = 0.462, P = 0.05), and between GBM thickness and HbA1c, serum total cholesterol and triglyceride levels (r = 0.60, P = 0.05; r = 0.789, P = 0.004; r = 0.70, P = 0.016, respectively), were observed. Glomerulomegaly as well as histological lesions resembling those of early diabetic nephropathy are observed in kidney biopsies of patients with morbid obesity even before the appearance of microalbuminuria. The potential regression of these changes after weight loss needs to be clarified.

Markers of Tubular and Glomerular Injury in Predicting Acute Renal Injury Outcome in Thermal Burn Patients: A Prospective Study

Background/aim. Thermal injury elicits several systemic consequences. Acute renal failure (ARF) is a well-known complication of severe burn and is an important factor leading to an increase in mortality. We aimed to focus on early diagnosis of acute renal failure occurring in major burns and to determine the predictors for acute renal failure. Subjects and methods. Forty patients with moderate to severe thermal burn injury—second- to third-degree with >20% of total body surface area—constituted the material of our study. The following parameters were recorded: age, sex, cause of the burn injury, burn surface of second and third degrees expressed as total body surface area burned in %, and Apache II score. All patients were subjected to routine investigations, including serum creatinine, blood urea nitrogen, fractional excretion of sodium, urinary malondialdehyde and microalbuminuria, completed on days 0, 3, 7, 14 and 21. Results. Nine patients (22.5% of all cases) developed acute renal failure, and four patients required supportive dialysis. The group that developed ARF showed rising markers of glomerular damage with appearance of microalbuminuria on day 0 that was maximal (3–4 times its normal level) at day 14 and constant with elevated serum creatinine, as well as burn size in the third week that progressed to overt proteinuria in three cases. Urinary malondialdehyde was also elevated before developing acute renal failure about three times their normal values, gradually increasing on day 14, associated with rising microalbuminuria followed by its decrease after controlling of septicemia. Two cases (22.2%) in ARF group who developed septicemia and required dialysis died on the 32nd and 36th days post-burn. Burn size and occurrence of septicemia were the only predictors of acute renal failure using multiple regression analysis (SE B 0.003 and 0.104; p value of 0.001 and .0371, respectively). Conclusions. Acute renal failure, which complicates 22.5% of burn patients, was found to be related to the size and depth of burn. Microalbuminuria and urinary malondialdehyde are useful markers for prediction of renal outcome in such group of patients. In our study. burn size and septicemia proved to be the only clinical parameters that predict renal outcome.