A systematic review of kidney transplantation from expanded criteria donors.

Since 1957, over 70 equations based on creatinine and/or cystatin C levels have been developed to estimate glomerular filtration rate (GFR). However, whether these equations accurately reflect renal function is debated. In this Perspectives article, we discuss >70 studies that compared estimated GFR (eGFR) with measured GFR (mGFR), involving ~40,000 renal transplant recipients and patients with chronic kidney disease (CKD), type 2 diabetes mellitus or polycystic kidney disease. Their results show that eGFR often differed from mGFR by ±30% or more, that eGFR values incorrectly staged CKD in 30-60% of patients, and that eGFR and mGFR gave different rates of GFR decline. Errors were unpredictable, and comparable for equations based on creatinine and/or cystatin C. We argue, therefore, that the persistence of these errors (despite intensive research) suggests that the problem lies with using creatinine and/or cystatin C as markers of renal function, rather than with the mathematical methods used for GFR estimation.

Estimated GFR: time for a critical appraisal.

https://www.kidney-international.org/article/S0085-2538(15)53045-7/pdf

CD14(++)CD16+ monocytes but not total monocyte numbers predict cardiovascular events in dialysis patients.

Two risk factors for the development and progression of cancers that are amenable to life style modification are chronic inflammation and the metabolic syndrome. This review proposes two new targets that may mechanistically integrate inflammation and metabolic syndrome, have been largely ignored, and are known to be druggable. Recent evidence has demonstrated that elevated serum uric acid (hyperuricemia) is associated with excess cancer risk, recurrence, and mortality. Although uric acid (UA) can function as a systemic antioxidant, its pro-inflammatory properties have been postulated to play an important role in the pathogenesis of cancer. Furthermore, obesity, Type 2 Diabetes Mellitus (T2DM), and the metabolic syndrome (MetS) are also associated with excess cancer, chronic inflammation, and with hyperuricemia, suggesting that UA may represent an important link between these disorders and the development of cancer. While pharmacological modulation of hyperuricemia could in principal augment anti-cancer therapeutic strategies, some cancer cells express low intracellular levels of the enzyme Xanthine Oxidoreductase (XOR) that are associated with increased cancer aggressiveness and poor clinical outcome. Thus, systemic pharmacological inhibition of XOR may worsen clinical outcome, and specific strategies that target serum uric acid (SUA) without inhibiting tumor cell XOR may create new therapeutic opportunities for cancer associated with hyperuricemia. This review will summarize the evidence that elevated SUA may be a true risk factor for cancer incidence and mortality, and mechanisms by which UA may contribute to cancer pathogenesis will be discussed in the hope that these will identify new opportunities for cancer management.

/pdf/contribution-of-uric-acid-to-cancer-risk-recurrence-and-2xizazu43j.pdf

Contribution of uric acid to cancer risk, recurrence, and mortality

Summary Background and objectives Measurement of C-reactive protein (CRP) levels remains uncommon in North America, although it is now routine in many countries. Using Dialysis Outcomes and Practice Patterns Study data, our primary aim was to evaluate the value of CRP for predicting mortality when measured along with other common inflammatory biomarkers. Design, setting, participants, & measurements We studied 5061 prevalent hemodialysis patients from 2005 to 2008 in 140 facilities routinely measuring CRP in 10 countries. The association of CRP with mortality was evaluated using Cox regression. Prediction of 1-year mortality was assessed in logistic regression models with differing adjustment variables. Results Median baseline CRP was lower in Japan (1.0 mg/L) than other countries (6.0 mg/L). CRP was positively, monotonically associated with mortality. No threshold below which mortality rate leveled off was identified. In prediction models, CRP performance was comparable with albumin and exceeded ferritin and white blood cell (WBC) count based on measures of model discrimination (c-statistics, net reclassification improvement [NRI]) and global model fit (generalized R 2 ). The primary analysis included age, gender, diabetes, catheter use, and the four inflammatory markers (omitting one at a time). Specifying NRI 5% as appropriate reclassification of predicted mortality risk, NRI for CRP was 12.8% compared with 10.3% for albumin, 0.8% for ferritin, and 0.1% for WBC. Conclusions These findings demonstrate the value of measuring CRP in addition to standard inflammatory biomarkers to improve mortality prediction in hemodialysis patients. Future studies are indicated to identify interventions that lower CRP and to identify whether they improve clinical outcomes. Clin J Am Soc Nephrol 6: ●●●–●●●, 2011. doi: 10.2215/CJN.00710111

/pdf/c-reactive-protein-and-prediction-of-1-year-mortality-in-1ufwe10zow.pdf

C-Reactive Protein and Prediction of 1-Year Mortality in Prevalent Hemodialysis Patients

Either inflammation or hyperuricemia has been related with increased cardiovascular risk and mortality. A hypothetical relationship between serum uric acid levels (SUA) and inflammatory markers has never been tested in chronic kidney disease (CKD) patients. The purpose of this study was to determine the prevalence of increased C-reactive protein (CRP) levels in CKD patients, and to test the hypothesis of a relationship between SUA and CRP levels. The study group consisted of 337 patients (174 males, mean age 63 +/- 16 years) with advanced chronic renal failure not yet on dialysis. None of them had overt inflammatory or infectious diseases. High sensitivity CRP levels were analyzed as a binary (above or below median value), or continuous variable (log-transformed CRP), by multiple logistic or linear regression analysis, respectively. Demographics, clinical, and biochemical characteristics, including SUA levels, were the variables tested in these analysis. In a subset of 169 patients without diabetes, the same analysis were carried out, with the inclusion of fasting insulin levels and HOMA-IR as independent variables. Median CRP level was 3.25 mg/L, and mean SUA level was 7.59 +/- 1.94 mg/dl. Patients with CRP levels above the median had significantly higher mean SUA level than that of the rest of study patients (7.93 +/- 1.79 vs 7.24 +/- 2.03 mg/dl, p = 0.001). SUA levels correlated significantly with log-transformed CRP levels (r = 0. 16, p = 0.0022). The relationship between SUA and CRP levels remained statistically significant after adjustment for age, sex, comorbid index, obesity, residual renal function, diuretic and allopurinol treatment, in the multivariate logistic and linear regression models (OR: 1.296, p = 0.0003; and beta: 0.204, p = 0.0002). The significant association between SUA and CRP levels did not change when HOMA-IR and fasting insulin levels were included as independent variables in the subset of 169 patients without diabetes. In conclusion, SUA levels are related with CRP levels in CKD patients.

[Serum uric acid and C-reactive protein levels in patients with chronic kidney disease].

Serum cystatin C (CysC) has been shown to be more accurate than serum creatinine (Cr) in estimating renal function, especially in patients with mildmoderate chronic renal failure. However, it is unknown whether CysC provides or not any advantage over Cr in severe chronic renal failure. The aim of this study was to establish the accuracy of CysC in estimating the glomerular filtration rate (GFR) in advanced chronic renal failure patients. The study group consisted of 94 patients (57 females, mean age 61 +/- 16 years) with advanced chronic renal failure. None of them had thyroid dysfunction or was on corticoid treatment. CFR was measured by TC99mDTPA, and simultaneously, serum CysC (particle enhanced immunonephelometry) and Cr (modified Jaffe's kinetic reaction) were also determined. Serum Cr and CysC levels were correlated with GFR, and the influences of age, sex and diabetes on these correlations were analyzed. The predictive value of CysC and Cr to estimate a GFR less than 15 ml/min/1.73 m2 was analyzed by measuring the crea-under-the-curve (AUC) with Receiver-Operating Characteristics (ROC) plots. The mean CFR was 16.49 +/- 4.65 ml/min/1.73 m2. The mean concentrations of Cr and CysC were 4.19 +/- 1.19 mg/L and 3.44 +/- 0.73 mg/L, respectively. Both Cr and CysC correlated significantly with GFR (R = 0.49, p < 0.0001 and R = 0.52, p < 0.0001, respectively). Age and sex influenced on the correlation between Cr and GFR, but these demographic characteristics did not influence on the correlation between CysC and GFR. The AUC for the prediction of a GFR less than 15 ml/min/1.73 m2 with serum Cr was 0.675 (p = 0.004), while with CysC was 0.633 (p = 0.030). In conclusion, both serum Cr and CysC are highly inaccurate markers of renal function in advanced chronic renal failure patients.

Cystatin C as estimator of glomerular filtration rate in patients with advanced chronic renal disease

Background. Elevated levels of inflammatory markers have been shown to be associated with increased mortality in chronic kidney disease (CKD) patients. Comorbid indexes are also helpful clinical instruments for predicting mortality. At present, it is unknown whether inflammatory markers add predictive information of death beyond that provided by comorbid indexes. Methods. This observational single-centre study included 404 patients (mean age 63 ± 16 years) with CKD stage 4 and 5 predialysis who were prospectively followed-up. Data obtained at baseline: demographics, grade of comorbidity by Davies index, serum albumin, creatinine clearance, total white blood cell (WBC), polymorphonuclear leukocyte (PMN) counts, and high-sensitivity C-reactive protein (CRP) were analysed as potential determinants of the subsequent all-cause mortality. Receiver-operating characteristic (ROC) curves were used to determine the values of CRP, WBC and PMN most closely related to mortality. These cut-off values were used to define subgroups with high or low inflammatory markers. Uni- and multivariate Cox regression models were performed. Results. Median follow-up time was 583 days, with a mortality of 26%, and overall survival rate of 47%. In unadjusted Cox models, inflammatory markers (CRP, WBC and PMN) were all significantly associated with all-cause mortality. Age (HR 1.05; 95% CI 1.03-1.07, P< 0.0001) and comorbid index (HR 2.15; 95% CI 1.54-3.00, P < 0.0001) were strongly associated with mortality. The introduction of inflammatory markers into the multivariate Cox regression model did not add significant predictive power. In a stepwise Cox model, the age, comorbid index, serum albumin levels and creatinine clearance were the best predictive variables of mortality. Conclusions. Although elevated inflammatory markers are associated with a worse outcome in CKD patients, they did not add predictive information of all-cause mortality beyond that provided by age and the comorbid index.

Do inflammatory markers add predictive information of death beyond that provided by age and comorbidity in chronic renal failure patients

Las ecuaciones de Cockcroft-Gault (CG) y MDRD son estimaciones indirectas
de la funcion renal de amplia aceptacion, pero que han sido escasamente validadas
en los estadios mas avanzados de la insuficiencia renal cronica (IRC). El
objetivo del presente estudio fue establecer la exactitud (sesgo y precision) de
estas estimaciones en pacientes con IR avanzada.
Se estudiaron 99 pacientes (59 mujeres, edad media 62 ± 15 anos), con IRC
avanzada predialisis. Se recogieron datos demograficos, comorbilidad, peso, talla,
creatinina, urea, y albumina. El filtrado glomerular (FG) se midio con Tc99m DTPA
(FG-DTPA). Simultaneamente se estimo el FG con las formulas de CG corregido
a 1,73 m2 y MDRD (formula 7). Se determino la exactitud de cada una de
las formulas analizando el grado de correlacion, sesgo (diferencia de media y
mediana), y precision (mediana de las diferencias absolutas y metodo de Bland-
Altman).
El FG-DTPA, y los estimados por CG y MDRD fueron respectivamente: 16,24
± 4,38; 16,77 ± 4,65 y 13,58 ± 4,27 ml/min/1,73 m2. FG-MDRD infraestimo significativamente
el FG-DTPA (p < 0,0001). La diferencia de la mediana fue mas
amplia con FG-MDRD (-3,24 frente 0,30 ml/min/1,73 m2, p = 0,0001), al igual
que la mediana de las diferencias absolutas (-3,11 frente 0,58 ml/min, p = 0,0001).
Los mejores determinantes del error FG-CG fueron: la creatinina (beta = -0,58; p
< 0,0001), la edad (beta = -0,62; p < 0,0001), y el indice masa corporal (beta
= -0,26; p = 0,004). Los mejores determinantes del error FG-MDRD fueron: creatinina
(beta = -0,38; p < 0,0001), y el indice masa corporal (beta = -0,20; p =
0,035).
En conclusion, en pacientes no seleccionados con IRC avanzada la estimacion
del FG con CG corregida a 1,73 m2 fue menos sesgada y mas precisa que con
MDRD. La creatinina serica fue la principal fuente de error en la estimacion del
FG con ambas formulas, aunque las caracteristicas demograficas y antropometricas
tambien influyeron.

Accuracy of indirect estimates of renal function in advanced chronic renal failure patients

The rate of oxalate absorbed from intestine is highly influenced by calcium intake in healthy subjects. It is unknown whether commonly used phosphate binders modify intestinal absorption and renal excretion of oxalate in chronic kidney disease (CKD) patients. This study aims to determine if calcium carbonate or sevelamer influences on urinary oxalate excretion. Twenty patients with CKD (stage 4 and 5 pre-dialysis) were included. Two treatment (1500 mg of calcium carbonate or 2400 mg of sevelamer), two-period (21 days each), crossover study with balanced assignment of the order of administration, and two washout periods were the main characteristics of this study design. Laboratory analyses in each phase included: serum creatinine, calcium, phosphorus, bicarbonate, total cholesterol, and 24 h urinary excretion of oxalate, creatinine, and urea. Creatinine clearance, protein catabolic rate (PNNA), total urinary oxalate excretion, and urinary oxalate / creatinine ratio were determined. Seventeen patients completed both treatment sequences. Total urinary oxalate excretion and urinary oxalate / creatinine ratios decreased significantly with respect to washout periods either after sevelamer or calcium carbonate treatment. The decrease in urinary oxalate excretion was greater after calcium carbonate (41.2+/-17.4%) than after sevelamer treatment (30.4+/-23.8%). There were not significant changes in renal function or PNNA values throughout the study periods. In conclusion, either calcium carbonate or sevelamer significantly reduces urinary oxalate excretion in CKD patients. Further studies will be needed to ascertain whether the type of phosphate binder influences on the accumulation of oxalate in CKD patients.

Either calcium carbonate or sevelamer decreases urinary oxalate excretion in chronic renal failure patients

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