Assessment of urinary N-acetyl-β-glucosaminidase as an early marker of contrast-induced nephropathy

Early detection and timely intervention are important for improving contrast-induced nephropathy (CIN) prognosis. Whether urinary N-acetyl-β-glucosaminidase (NAG) is a useful marker for early detection of CIN was investigated in 590 patients undergoing diagnostic coronary angiography (CA) and/or therapeutic percutaneous coronary intervention (PCI) for acute coronary syndromes or stable angina, and who received low-osmolality nonionic contrast agent. Urinary NAG, osmolality and serum creatinine were measured before and 1, 2 and 6 days after contrast agent exposure. CIN occurred in 33 patients; its incidence in high-risk patients (pre-existing renal dysfunction with/without diabetes mellitus) was significantly higher than in others. In patients with CIN, urinary NAG and serum creatinine levels on days 1 and 2 were significantly higher than at baseline and compared with patients without CIN; mean levels were gradually returning to baseline by day 6. Compared with serum creatinine, urinary NAG levels peaked earlier in CIN patients and increased much more. The results suggest that, following CA and/or PCI, CIN occurs to a certain degree and that NAG may be a useful early CIN marker as it is noninvasive, simple, inexpensive and sensitive.     

Correlation between restrict of protein intake and diabetic nephropathy

Background：Diabeticnephropathyisoneofseverecomplica－tionsofdiabetesmellitus（DM）．WiththeincreasingofincidenceofDM，diabeticnephropathy（DN）hasbecomethemostcommoncauseofrenalfailureintheendstage．Moreandmorepatientreceivetreatmentofdialysisandkidneytransplantation．TheeffectofproteinintakeonpathophysiologyofDNhasbeentakenmoreandmoreseriously．Studieshaveshownthatrestrictionofproteinintakecoulddelaytheprogressofrenalfailure，relievesymptomsofuremia，andprovidegoodprognosisofDN．Objecti…     

Is urinary 5-hydroxyindoleacetic acid helpful for early diagnosis of acute appendicitis?

Objective

Acute appendicitis is the most common abdominal emergency in children and young adults. There are a lot of serotonin-containing cells in the appendix, which release serotonin into the bloodstream in response to inflammation. Consequently, serotonin is converted to 5-hydroxyindoleacetic acid (5-HIAA) and secreted into the urine. On this basis, urinary 5-HIAA could be a marker for acute appendicitis. In this study, we investigated the value of 5-HIAA levels in spot urine in the diagnosis of acute appendicitis.

Methods

The urinary 5-HIAA was measured by an enzyme-linked immunosorbent assay in the spot urine of 70 patients who presented to the emergency department with a clinical picture of acute appendicitis. Urine concentration results were correlated to final histopathologic reports, and the diagnostic value of this factor was measured.

Results

Diagnosis of appendicitis was confirmed by histopathologic reports in 59 of 70 patients with presumptive diagnosis of appendicitis. Considering 5.25 mg/L as the cutoff point for urinary 5-HIAA, 28 patients had high urinary 5-HIAA levels, whereas 42 patients had values within reference range. The sensitivity and specificity of this test was 44% and 81%, respectively.

Conclusions

The measurement of urinary 5-HIAA levels is not an ideal diagnostic tool for ruling out or determination of acute appendicitis.     

Noninvasive tool for the diagnosis of polyomavirus BK–associated nephropathy in renal transplant recipients

Noninvasive methods can facilitate early diagnosis of BK virus (BKV) replication and guide the evaluation of BKV-associated nephropathy (BKVAN). We developed 3 noninvasive methods for BKVAN screening including quantitative polymerase chain reaction (PCR) assay for BKV DNA load in urine and plasma, and quantitative assay of urine cytology by light microscopy or electron microscopy, and used these assays concurrently with renal transplant biopsies for the evaluation of 338 patients. BKVAN was diagnosed in 24 (7.1%) of 338 renal recipients. The median level of the 3 methods was the highest in pattern B of BKVAN (P < 0.05). Using these 3 methods for pattern B of BKVAN yielded a high sensitivity of 100%. Using decoy cells without quantitation had a sensitivity of 95.8% and a specificity of 83.1% for BKVAN. The amount of decoy cells in urine samples was related to BKV DNAuria, BKV DNAemia, and the pattern of BKVAN. Using a decoy cell threshold of >5 per 10 high-power fields (HPF) had an ideal sensitivity and specificity for high-risk BKVAN and BKVAN. Using a decoy cell threshold of >20 per 10 HPF for BKVAN had a specificity of 99.7%. Quantitative assay of urine cytology is a very convenient and sensitive method for diagnosis of BKVAN, which can be deemed as an additional diagnostic method for quantitative PCR screening with increased accuracy.     

Assessment of PI-RADS v2 categories ≥ 3 for diagnosis of clinically significant prostate cancer

Abdominal Radiology - To assess the diagnostic accuracy of PI-RADS v2 categories ≥ 3 to detect clinically significant prostate cancer (csPCa) against histopathology of...     

Urinary matrix metalloproteinase-8 and -9 activities in type 2 diabetic subjects: A marker of incipient diabetic nephropathy?

Matrix metalloproteinases (MMPs) may play a pathophysiological role in the development of diabetic nephropathy (DN). We hypothesized that urinary MMP activity in patients with type 2 diabetes mellitus (T2DM) is related to a decline in renal function. We determined MMP-2, -8 and -9 activity in 24-h urine collections in relation to risk factors for DN in T2DM patients with (UA, n = 27) and without albuminuria (NA, n = 48) and controls (CO, n = 28). MMP-8 and -9 levels were highest in UA patients (P < 0.01). Of UA patients, 93% had at least one MMP increased, compared to 78% of NA patients and 46% of CO (P = 0.001). Age, diabetes duration, BMI, systolic blood pressure, fasting plasma glucose, HbA1c and renal function were determinants of MMP-8 and -9 (P < 0.05). In summary, MMP-8 and -9 are highest in T2DM UA patients. MMP-9, showed the strongest associations with clinical parameters related to DN.     

Vascular endothelial dysfunction: A tug of war in diabetic nephropathy?

Vascular endothelium regulates vascular tone and maintains free flow of blood in vessels. Vascular endothelial dysfunction (VED) results in reduced activation of endothelial nitric oxide synthase (eNOS), reduced generation and bioavailability of nitric oxide (NO) and increased production of reactive oxygen species (ROS). The eNOS uncoupling in VED leads to eNOS mediated production of ROS that further damage the endothelial cells by upregulating the proinflammatory mediators and adhesion molecules. VED has been associated in the pathogenesis of hypertension, atherosclerosis, coronary artery diseases, diabetes mellitus and nephropathy. Diabetes is a chronic metabolic disorder characterized by hyperglycemia followed by micro and macrovascular complications. A correlation between diabetes and VED has been demonstrated in various studies. The downregulation of eNOS in diabetes has been noted to accelerate diabetic nephropathy. Moreover, various endogenous vasoconstrictors are also upregulated in diabetic nephropathy. VED has been shown to be involved in diabetic nephropathy by inducing nodular glomerulosclerosis followed by glomerular basement membrane thickness and mesangial expansion, which ultimately decline glomerular filtration rate (GFR). Thus it is suggested that diabetes-induced VED could be one of the culprits involved in the pathogenesis of diabetic nephropathy.     

Assessment of the SD Bioline Ag MPT64 Rapid™ and the MGIT™ TBc identification tests for the diagnosis of tuberculosis

Successful control of tuberculosis relies on the rapid detection of Mycobacterium tuberculosis. Few chromatographic lateral flow assays for the discrimination of the M. tuberculosis complex were developed from culture media. We compared the values of 2 assays to assess their place in diagnosis of tuberculosis. We conclude of their efficiency and relevance to supplant the conventional methods.     

What is the impact of PRIME on real‐life diabetic nephropathy?

Type 2 diabetes is increasing globally and is a major cause of conditions such as cardiovascular disease, retinopathy and nephropathy. The Diabetes Control and Complications Trial and the UK Prospective Diabetes Study demonstrated that the progression of renal disease could be slowed by tight glycaemic control and treating any associated hypertension with angiotensin-converting enzyme inhibition. Recent clinical trials have supported the use of angiotensin II receptor antagonists in the treatment of diabetic nephropathy, resulting in the approval of new therapeutic indications in the United States and Europe. The objective of this review is to demonstrate how results from the Program for Irbesartan Mortality and morbidity Evaluation studies apply to clinical practice, and to show how the benefits of irbesartan therapy can be realised at any stage of renal disease in patients with diabetes.     

Effect of RAS inhibition on TGF-β, renal function and structure in experimentally induced diabetic hypertensive nephropathy rats

Objective

Transforming growth factor-β (TGF-β) implicated in the pathogenesis of diabetic nephropathy. Hence, developing agents that antagonize fibrogenic signals is a critical issue facing researchers.

Material and methods

Fifty rats were allocated to five groups: 1 = control rats, 2 = diabetic hypertensive rats 3 = diabetic hypertensive rats treated with spironolactone, 4 = diabetic hypertensive rats treated with moexpril, 5 = diabetic hypertensive rats treated with both spironolactone and moexpril. Measurement of TGF-β, aldosterone, creatinine and ACE. Degree of fibrosis was calculated.

Results

Serum creatinine, mean arterial blood pressure (MAP), aldosterone, ACE, TGF-β and renal fibrosis increased significantly in untreated diabetic hypertensive rats compared with control rats. Administration of spironolactone, moexpril, or both decreased these changes.

Conclusions

Addition of the spironolactone to moexpril was more effective in reducing fibrosis and improvement of renal function than monotherapy with either drug, possibly due to a dual inhibitory effect on the RAS, and thus suppression of TGF-β.     

Can intensive treatment alter the progress of established diabetic nephropathy to end-stage renal failure?

Diabetic nephropathy is now the leading cause of end-stage renal disease in the Western world, and is associated with a higher patient morbidity and mortality than other causes of renal failure, largely because of associated cardiovascular disease. Numerous studies have elucidated the factors which influence its onset and progression. The St Vincent Declaration in 1994 proposed standards for the appropriate management of patients with diabetic nephropathy. We assessed whether referral to a nephrology clinic attempting to apply these standards influenced the progression of diabetic nephropathy. The results show a significant improvement in blood pressure, glycosylated haemoglobin and serum cholesterol following referral. There was a significant reduction in the rate of decline of renal function following referral in 39% of patients. With the possible exception of diabetic control there were no significant differences in the management of those that did and did not show improvement. The results show that with intensive out-patient clinic monitoring it is possible to improve the quality of patient care, and that even in established diabetic nephropathy it is possible to slow the rate of progression to end-stage renal failure.     

Are the TASC recommendations for diagnosis and treatment of PAOD still relevant?

With regards to the rapid progress of interventional therapy in the treatment of PAOD the revision of the published guidelines (TASC Recommendations 2000) is more than necessary. The current options in therapy are modified constantly. Therefore, published recommendations might be not up-to-date. In consideration of the number of interventions and operations which are performed throughout Europe a trend towards less invasive treatment becomes apparent. Guidelines and recommendations from the Charing Cross and the ACC/AHA (ACC/AHA Guidelines for the Management of Patients With Peripheral Arterial Disease 2005) are reflecting this development. Regardless of the complexity of the planned procedure interventional treatment is almost always first choice therapy. A yearly revision of the actual guidelines would be useful, leading to an up-to-date modality. Although in the diagnostic pathway MRI and CTA gain more importance, the gold standard in diagnosis of PAOD remains the standardised measurement of the walking capacity, ankle-brachial index (ABI) and duplex ultrasound.