The 2011 Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury (AKI) aims to assist practitioners caring for adults and children at risk for or with AKI, including contrast-induced acute kidney injury (CI-AKI). Guideline development followed an explicit process of evidence review and appraisal. The guideline contains chapters on definition, risk assessment, evaluation, prevention, and treatment. Definition and staging of AKI are based on the Risk, Injury, Failure; Loss, End-Stage Renal Disease (RIFLE) and Acute Kidney Injury Network (AKIN) criteria and studies on risk relationships. The treatment chapters cover pharmacological approaches to prevent or treat AKI, and management of renal replacement for kidney failure from AKI. Guideline recommendations are based on systematic reviews of relevant trials. Appraisal of the quality of the evidence and the strength of recommendations followed the GRADE approach. Limitations of the evidence are discussed and specific suggestions are provided for future research.

A rare form of genetic mitochondrial nephropathy due to the deficiency of Coenzyme Q₁₀ that is often accompanied with multisystem disorders is reviewed. The diagnosis is based upon molecular genetic studies and the presence of multiple dysmorphic mitochondria in podocytes, mesangial and endothelial cells revealed by electron microscopy. Early diagnosis is mandatory since some forms of nephrotic syndrome may respond to the treatment with Coenzyme Q₁₀.

Studies of the role of methylarginines (MA) in the regulation of nitric oxide (NO) bioavailability showed that monomethylarginine (MMA) and asymmetric dimethylarginine (ADMA) competitively inhibit NO-synthase (NOS). Symmetric dimethylarginine (SDMA) is not active in respect of NOS. It however regulates transmembrane transport of L-arginine – a NOS substrate. High MA concentration in blood MA was shown to depresses many vascular functions which depend on NO. High level of MA contributes to the development of atherosclerosis and hypertension. Blood concentrations of MA, serotonin (5-HT), its metabolite (5-HIAA) and catecholamines were measured using HPLC with electrochemical and fluorometric detectors in healthy individuals and hemodialysis patients. The levels of ADMA, MMA and SDMA were significantly higher in hemodialysis than in control group. Hemodialysis reduced these levels, but not completely restored their normal values. Level of 5-HT in platelet-poor plasma was 6 times higher, and 5-HIAA was almost 30 times higher in hemodialysis patients than in the control group. Dialysis had no effect on plasma arginine and platelet 5-HT. Significant correlations were found between monoamines and methylarginines in hemodialysis patients, but not in the control group. Our data suggest that vascular pathology in hemodialysis patients could not be attributed to any systems studied. One should keep in mind their interaction and mutual substitution. Our and literature data allow one to assume that negative correlation between arginine and norepinephrine reflects the peculiarities of reaction to the medication stress which are characteristic for hypertensive patients. This work was supported by RFBR grant 08-04-00951.

Screening of the Almaty-city population for chronic kidney disease (CKD) in was performed by the Kazakhstan Nephrology Association with support of health authority on 19–28 February, 2009. In total 4054 adults and 556 children were inspected. Blood pressure, height and weight, urine express test (using strips), serum creatinine level with calculation of glomerular filtration rate (GFR) were assessed. CKD 3 was revealed at 6% of adults and 1,68% of children and teenagers, i.e. the frequency of CKD in Kazakhstan exceeds average world level. The role of arterial hypertension and diabetes in CKD occurrence was revealed.

Thrombotic thrombocytopenic purpura (TTP) is a rare life-threatening disorder characterized by microangiopathic hemolytic anemia, thrombocytopenia, neurological and renal abnormalities and fever. The pathogenesis TTP is related to a severe deficiency of specific metalloprotease, ADAMTS 13 (a disintegrin and metalloprotease with thrombospondin type I motif 13) that cleaves the largest von Willebrand factor multimers in plasma and prevents the spontaneous formation of platelet thrombi in the microcirculation. Prognosis of TTP has been improved by plasma therapy decreasing the mortality rate from 90% to less than 20%. A case of severe acute TTP in 39-year-old woman, successfully treated with repeated plasma exchange is presented. Recent data on pathogenesis and treatment of TTP are briefly reviewed.

Thrombotic kidney microangiopathy is a special kidney disease of vascular origin. Its diagnostics became possible only recently thanks to the development and advancement of diagnostic puncture nefrobiopsy. The differention between primary and secondary forms of thrombotic microangiopathy kidney are very important for a clinician as well as the ability to allocate its hereditary forms by studying gene polymorphisms. We present clinical observations of thrombotic microangiopathy kidney as the single clinical manifestation of hereditary thrombophilia.

Fungous infections in post-transplant period cause serious problems worldwide. Combined fungal infection invasive candidosis and invasive aspergillosis of the transplant, often lead to the loss of the renal transplant. The early diagnostics and start of treatment are extremely important and vitally necessary. We report a case of successful treatment of fungous infection that caused urological complication in a renal transplant recipient.

We present an observation of early-onset steroid-resistant nephrotic syndrome with sensorineural deafness as a consequence of CoQ₁₀ deficiency, with ultrastructural renal lesion characterized by widespread proliferation of abnormal mitochondria in glomerular cells.