PURPOSE:

We propose a simple and inexpensive in vitro crystallization assay of measuring turbidity by spectrophotometry in synthetic urine. We validated our method by investigating the effect of potassium (K) citrate on the crystallization of calcium oxalate monohydrate (CaOx), calcium phosphate, and magnesium ammonium phosphate using synthetic urine.

METHODS:

The crystallization of CaOx was studied using turbidimetric measurements of solution produced by mixing calcium chloride and sodium oxalate at 37 °C, pH 5.7. The turbidity of the crystal suspension was measured immediately with double-beam spectrophotometer as the absorbance of light at 660 nm wavelength. The rates of crystal formation and aggregation were obtained by measuring optical density (OD) over 30 min. The obtained results were compared to CaOx crystal concentration with and without citrate assessed by optical microscopy.

RESULTS:

The sensitivity of spectrophotometry in measuring turbidity was confirmed by the linear correlation between the crystal concentration and OD readings at 660 nm seen on the standard curve. Under similar experimental conditions, the results were comparable to the ones obtained by optical microscopy. The OD readings over 30 min revealed an instant decrease in the number of crystals, with maximum aggregation noted at 18 min. Addition of K-citrate at 1.25 mg/ml led to initial less crystal formation (OD = 0.236 nm vs. OD = 0.527 nm), with a maximum aggregation reached at 18 min. Overall, citrate addition decreased nucleation with a small change in the aggregation (OD = 0.316 vs. OD = 0.359).

CONCLUSION:

Spectrophotometric measurement of urinary turbidity is feasible and sensitive in assessing the potential clinical usefulness of different medications in inhibiting crystallization in urine.

PURPOSE:

Sensitization to HLA antigens resulting in anti-HLA antibodies (panel reactive antibodies; PRA) is a major problem in chronic kidney disease (CKD) patients awaiting transplantation. Induction of anti-HLA antibodies normally occurs through blood transfusion, pregnancy and prior transplantation. However, some patients develop these antibodies for unknown immunological reasons. It is hypothesized that deviations in immune regulation may account for PRA positivity in these patients. We, therefore, investigated whether a quantitative deficiency in peripheral natural regulatory T cells (CD4(+)CD25(high)Foxp3(+); nTreg) plays a role in this phenomenon.

METHODS:

Peripheral blood mononuclear cells from 14 patients with positive (Class I and Class II; 10-100 %) and 25 patients with negative PRA, who had not previously been sensitized by blood transfusion, pregnancy and prior transplantation and who had not received any immunomodulatory treatment within the last year, were analyzed for absolute lymphocyte and nTreg numbers through flow cytometry. Samples from 10 healthy people were also used as control.

RESULTS:

Mean absolute nTreg numbers were determined to be severely reduced in CKD patients (12 ± 9; n = 39) compared with healthy individuals (53 ± 17; n = 10) (p = 0.008). However, absolute nTreg numbers were similar between PRA- (12 ± 11) and PRA+ (11 ± 8) groups. Interestingly, there was a moderate correlation between the nTreg numbers and HLADR2 genotype (n = 9, r = 0.508, p < 0.05).

CONCLUSION:

This is the first study to demonstrate that the quantitative peripheral nTreg deficiency in CKD patients does not show a causal relationship with the presence of anti-HLA antibodies.

Acute kidney injury (AKI) is a very frequent and serious clinical problem, accounting for overall high morbidity and mortality. Up to date, mortality due to AKI is virtually unchanged over the past 50 years. This may partly be explained due to a delay in initiating renal protective and appropriate therapeutic measures since until now there are no reliable early-detecting biomarkers. The gold standard, serum creatinine, displays poor specificity and sensitivity with regard to identification of the incipient phase of AKI, and this is also true for cystatin C. We aimed to review novel biomarkers of AKI in urine and serum which have now progressed to the clinical phase. The main focus refers to their diagnostic and prognostic value. For this purpose, a web-based literature search using PubMed was performed comprising the following terms: renal failure, acute kidney injury and biomarkers. New molecules such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), monocyte chemotactic peptide (MCP-1), Il-18, liver-type fatty acid-binding protein (L-FABP) and Netrin-1 are available and represent promising new markers that, however, need to be further evaluated in the clinical setting for suitability. In clinical settings with incipient AKI, not only the development and the implementation of more sensitive, practicable and accurate biomarkers are required for well-timed treatment initiation. Just as important is a substantial improvement of refined and applicable prophylactic therapeutic options in these situations. Before full adoption in clinical practice can be accomplished, adequately powered clinical trials testing a row of biomarkers are strongly warranted.

BACKGROUND:

Incretin hormones are secreted in the gut after a meal and stimulate insulin production. Both major incretins, that is, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are eliminated by the kidneys. Little is known about the influence of end-stage renal disease (ESRD) on the incretin axis. The aim of the study was to assess the effect of the commencement of chronic hemodialysis (HD) therapy on serum GLP-1 and GIP, and insulin sensitivity in diabetic and non-diabetic patients.

SUBJECTS AND METHODS:

The study comprised 56 patients (23 F, 33 M; mean age 57 ± 14 years) with ESRD in the course of diabetic nephropathy (n = 23) and non-diabetic renal diseases (n = 34) who started chronic HD. Glucose metabolism, including incretin hormones concentration, was assessed before the first HD session and repeated after the first 6 months of the therapy.

RESULTS:

After 6 months of HD, a significant increase in fasting GLP-1 concentration was observed in both diabetic and non-diabetic patients [by 2.27 pmol/l (45 %) and 1.28 pmol/l (22 %), respectively, p = 0.0003]. Serum GIP increased significantly only in diabetic patients [by 30.9 pg/ml (55 %); p = 0.008]. No significant change of fasting glucose was found but HOMA-IR and serum insulin decreased significantly in diabetic patients (p = 0.01 and p = 0.008, respectively). In contrast, HOMA-B was unchanged in both groups. Changes of HOMA-IR did not significantly correlate with serum GLP-1 or GIP concentrations.

CONCLUSION:

Our results indicate that starting the hemodialysis therapy helps to restore the incretin axis in particular in patients with the diabetic kidney disease.

PURPOSE:

To assess the impact of the number of lymph nodes removed and of the template of dissection during radical cystectomy for bladder cancer on patients' survival rates.

MATERIALS AND METHODS:

We evaluated 282 consecutive patients who underwent radical cystectomy for muscle-invasive or high-grade superficial bladder cancer between 1995 and 2011. Exclusion criteria were incomplete follow-up data and neo-adjuvant or adjuvant treatments. Patients were divided into groups according to the most informative cut-point of number of lymph nodes retrieved and of the template of dissection. The cancer-specific survival rates were estimated by the Kaplan-Meier method. The univariate and multivariable forward-stepwise Cox proportional hazards regression were applied to analyze the survival outcomes.

RESULTS:

The mean (SD) follow-up was 59.2 ± 44.3 months, and the mean (SD) age of the entire cohort population was 68.3 ± 8.3 years. The cancer-specific survival rates were 58.7 and 47.7 % at 5 and 10 years, respectively. Considering both node-positive and node-negative patients, those with at least 14 LNs removed and those submitted to extended or super-extended PLND experienced significantly higher cancer-specific survival at both univariate and multivariable analysis.

CONCLUSIONS:

Patients undergoing a more extended pelvic lymph node dissection, both in terms of number of LN removed and in terms of template of dissection, will experience a better cancer-specific survival. Our data support a potential role of lymphadenectomy on cancer outcome.

PURPOSE:

The optimal management of patients with ureteric obstruction in advanced pelvic malignancy is unclear. Effective judgment is required to decide which patients would benefit most from decompression of the urinary tract. The objective of our study was to assess survival and complication rates post-percutaneous nephrostomy (PCN) in patients with ureteric obstruction due to advanced pelvic malignancy.

METHODS:

A detailed retrospective case review of all patients who underwent PCN for ureteric obstruction due to pelvic malignancy in one calendar year was conducted to assess indication, survival time, length of stay post-procedure and complications.

RESULTS:

Thirty-six nephrostomies were performed on 22 patients with prostate cancer being the commonest primary (55 %). Renal failure was the commonest mode of presentation (56 %). Eight patients (36 %) presented without a prior diagnosis of cancer. All PCNs except one were initially technically successful, and 56 % of renal units were able to be antegradely stented and rendered free of nephrostomy. Median survival post-nephrostomy was 78 days (range 4-1,137), with the subset of bladder cancer patients having the poorest survival. Dislodgement of the nephrostomy tube was the most common troublesome complication which led to the greatest morbidity, sometimes requiring repeat nephrostomy insertion. Patients stayed for a median of 23 (range 3-89) days in hospital, which amounted to 29 % of their remaining lifetime spent in hospital.

CONCLUSIONS:

Although effective in improving renal function, PCN is a procedure not without associated morbidity and does not always prolong survival. Therefore, the decision to decompress an obstructed kidney with advanced pelvic malignancy should not be taken lightly. We recommend that such cases be discussed in a multidisciplinary setting, and a decision is taken only after a full informed discussion involving patients and their relatives.

AIMS:

Prostate cancer is very common and is the second most common cause of cancer death in males in Australia; however, brain metastases are exceedingly rare.

MATERIALS AND METHODS:

We review four cases of biopsy-proven brain metastases from prostate cancer and review the relevant literature.

RESULTS:

Three of four patients had acinar adenocarcinoma of prostate with one patient having ductal adenocarcinoma variant on histopathology. Three patients had the brain as the only site of metastatic disease. All patients underwent surgery, and three of four patients underwent adjuvant palliative radiotherapy to the brain.

CONCLUSION:

Brain metastases from prostate cancer are rare, but brain metastases without other sites of metastatic disease are exceedingly rare and may be more common with ductal adenocarcinoma variant.