Three cases of polycystic kidney were treated with conservative therapy. Of three cases one showed normal blood pressure and improved digestive disturbance after the therapy. i. e., direct aspiration of the kidney. Direct aspiration method is thought to be desirable one before the kidney operation is performed.
Blood Pressure ; Kidney ; Polycystic Kidney Diseases*

BACKGROUND: Few data showed the optimal blood pressure (BP) in noncritically ill patients with acute kidney injury (AKI) relative to mortality or severe AKI. We therefore sought to analyze the data that exist for the ideal target range for BP in noncritically ill patients with AKI. METHODS: We performed a retrospective cohort study involving 1,612 hospitalized patients who were diagnosed with AKI using the Kidney Disease: Improving Global Outcomes definition based on serum creatinine measurements for a period of 1 year. The average systolic BP (SBP) was categorized into 10-mmHg increments (within 48 hours after the development of AKI). The primary outcome was a composite of severe AKI or 90-day mortality. RESULTS: The composite outcome rate in patients was 18.7% (302/1,612). The relationship between BP and the composite outcome followed a U-shaped curve, with an increased event rate observed at both low and high BP values. The average SBP after AKI predicted the composite outcome after adjusting for baseline variables (reference SBP: 120–129 mmHg; < 100 mmHg: hazard ratio [HR] 1.84, P = 0.015; 100–109 mmHg: HR 1.56, P = 0.038; 110–119 mmHg: HR 1.15, P = 0.483; 130–139 mmHg: HR 1.51, P = 0.045; ≥ 140 mmHg: HR 1.73, P = 0.005). CONCLUSION: Among noncritically ill patients with AKI, a U-shaped curve association was observed between the average SBP within 48 hours after AKI and the composite primary outcome of this study, with the lowest event rate for SBP ranging from approximately 110 to 129 mmHg.
Acute Kidney Injury ; Blood Pressure ; Cohort Studies ; Creatinine ; Humans ; Kidney Diseases ; Mortality ; Retrospective Studies

Hypertension affects the majority of patients with chronic kidney disease (CKD) and increases the risk of cardiovascular disease, end-stage renal disease and mortality. Previously, many hypertension guidelines have suggested blood pressure targets in patients with CKD. Recently, the American College of Cardiology/American Heart Association 2017 Guideline for Hypertension suggests a new definition for hypertension and therapeutic targets, which were equally applicated to patients with CKD. These changes reflect the results of the Systolic Blood Pressure Intervention Trial (SPRINT) study, but the renal outcome of intensive blood pressure control was not good. Furthermore, the majority of hypertension guidelines including those of the Korean Society of Hypertension and the European Society of Hypertension have retained the traditional definition. Herein, we intend to analyze in detail the effect of intensive blood pressure control on kidney through the post-hoc analyses of the SPRINT study.
Blood Pressure ; Cardiovascular Diseases ; Diagnosis ; Heart ; Humans ; Hypertension ; Kidney ; Kidney Failure, Chronic ; Mortality ; Renal Insufficiency, Chronic

Diabetic nephropathy is the leading cause of end-stage renal disease, and is associated with increased risk of cardiovascular disease. Optimal control of blood glucose and blood pressure based on the blockade of renin-angiotensin system is the standard of care for the prevention and treatment of diabetic nephropathy. Regardless of these therapies, the prevalence of diabetic nephropathy continues to increase, highlighting the need for additional therapies. Diabetes affects the progression of kidney disease through a variety of mechanisms; several new therapeutic agents targeting these pathways have been developed, with currently being evaluated in clinical trials.
Albuminuria ; Blood Glucose ; Blood Pressure ; Cardiovascular Diseases ; Diabetic Nephropathies* ; Diagnosis ; Kidney Diseases ; Kidney Failure, Chronic ; Prevalence ; Renal Insufficiency, Chronic ; Renin-Angiotensin System ; Standard of Care

OBJECTIVEThe analyze the correlation of heart and kidney biomarkers to different heart and kidney diseases and explore the pathogenesis and classification of cardiorenal syndrome.

METHODSThis study involved 841 consecutive patients (600 males and 241 females) admitted between January, 2008 and May, 2008, who underwent NT-ProBNP and creatinine tests during hospitalization. The patients were classified according to the clinical diagnosis at the admission and to the status of the heart and kidney biomarkers.

RESULTSThe heart and kidney biomarkers were significantly different between genders. NT-proBNP showed slight elevations in patients with atrial fibrillation, mild non-heart disease, hypertension and angina, but significant elevation in patients with severe non-heart disease. In patients with renal artery stenosis, the heart and kidney biomarkers were moderately increased, which was also seen in patients with diabetes mellitus, myocardial infarction and coronary artery bypass grafting. In dilated cardiomyopathy and rheumatic heart disease, NT-proBNP showed marked increase with only slight increase of creatinine. Patients with chronic kidney disease had the highest NT-proBNP and creatinine levels and the lowest eGFR. The heart and kidneys index increased with the severity of the disease. From Ronco type I to type IV, NT-proBNP rose gradually, but the difference was not statistically significant (P>0.05), and the type I and IV patients had the highest creatinine level; type III involved mainly acute coronary syndrome, heart failure and renal stenosis. According to a modified classification, cardiarenal syndrome was characterized mainly by a marked increase of NT-proBNP, while renalcardiac syndrome by creatinine increases (P<0.05). Acute coronary syndrome, heart failure and renal artery stenosis represented a special entity of cardiorenal syndrome.

CONCLUSIONSHeart and kidney biomarkers and clinical diagnosis are closely related. The heart and kidneys index more accurately reflects the severity of the cardiorenal syndrome. The heart and kidney biomarkers can be used in Ronco classification. The simplified classification is convenient to use and facilitates the clinical decisions of the treatment.

Aged ; Aged, 80 and over ; Biomarkers ; blood ; Female ; Heart Diseases ; blood ; complications ; diagnosis ; Humans ; Kidney Diseases ; blood ; complications ; diagnosis ; Male ; Middle Aged ; Natriuretic Peptide, Brain ; blood ; Syndrome

Changes in renal function are one of the most common manifestations of severe illness. There is a clinical need to intervene early with proven treatments in patients with potentially deleterious changes in renal function. Unfortunately progress has been hindered by poor definitions of renal dysfunction and a lack of early biomarkers of renal injury. In recent years, the definitional problem has been addressed with the establishment of a new well-defined diagnostic entity, acute kidney injury (AKI), which encompasses the wide spectrum of kidney dysfunction, together with clearer definition and sub-classification of the cardio-renal syndromes. From the laboratory have emerged new biomarkers which allow early detection of AKI, including neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C. This review describes the new concepts of AKI and the cardio-renal syndromes as well as novel biomarkers which allow early detection of AKI. Panels of AKI biomarker tests are likely to revolutionise the diagnosis and management of critically ill patients in the coming years. Earlier diagnosis and intervention should significantly reduce the morbidity and mortality associated with acute kidney damage.
Acute Kidney Injury/*diagnosis ; Biological Markers/analysis/blood/urine ; Cystatin C/blood/urine ; Heart Failure/complications/etiology ; Humans ; Kidney Diseases/complications/*diagnosis/etiology ; Lipocalins/blood/urine ; Syndrome

BACKGROUNDvon Willebrand factor (vWF) mediates the initial capture of platelets to vascular subendothelium and is essential for platelet aggregation under high fluid shear stress as in arterial stenosis. On release from endothelial cells, vWF is rapidly cleaved by ADAMTS13/vWF-cleaving protease (vWF-CP). We investigated the clinical significance of changes in plasma vWF and vWF-CP activities in chronic renal disease.

METHODSPlasma vWF and vWF-CP activities were measured using enzyme-linked immunosorbent assay (ELISA) and residual collagen binding assay respectively in patients with lupus nephritis (n = 31), primary nephritic syndrome (n = 25), diabetic nephropathy (n = 45), chronic glomerulonephritis (n = 38) and 40 normal controls. The relation of their levels with pathological and renal status was analyzed.

RESULTSIn all diseased patients the levels of vWF were significantly higher and vWF-CP activity significantly lower than the controls (both P < 0.01). vWF in the four subgroups did not correlate with the stage of disease but correlated negatively with vWF-CP activity. vWF-CP activity was not changed two weeks after renal transplantation. Renal biopsy demonstrated that the vWF level in stage IV was higher than in stages II and III while vWF-CP activity was lower in patients with lupus nephritis. After eight-week treatment, the vWF level significantly decreased and the vWF-CP activity significantly increased in systemic lupus erythema, disease activity index < 9, but not with index = 9. Even though the vWF-CP activity was significantly lower in membranous nephropathy than in minimal change disease, mesangial proliferative glomerulonephritis or IgA glomerulonephritis, the vWF level was not significantly different.

CONCLUSIONSThe alterations of plasma vWF and vWF-CP activities were associated with different renal pathologies. Injury to endothelial cells and autoantibodies against vWF-CP activity may result in higher vWF level and lower vWF-CP activity in chronic renal disease and thus a mechanism for worsening of chronic renal disease and thrombosis.

ADAM Proteins ; blood ; ADAMTS13 Protein ; Adolescent ; Adult ; Aged ; Chronic Disease ; Female ; Humans ; Kidney Diseases ; blood ; Kidney Transplantation ; Lupus Nephritis ; blood ; Male ; Middle Aged ; von Willebrand Factor ; analysis

Adolescent ; Apolipoproteins E ; blood ; Humans ; Hyperlipoproteinemias ; complications ; Hypolipidemic Agents ; therapeutic use ; Kidney Diseases ; blood ; drug therapy ; pathology ; Kidney Glomerulus ; blood supply ; pathology ; Male ; Thrombosis ; pathology

OBJECTIVETo identify potential mutation of apolipoprotein E (apoE) gene in a male patient affected with lipoprotein glomerulopathy (LPG), his mother and his sister.

METHODSThe patient and his mother both had histologically confirmed LPG. His sister and his father were asymptomatic. Genomic DNA was extracted from peripheral blood samples. PCR products of the coding region of exons 3 and 4 of the apoE gene were cloned into a pTA2 vector and sequenced. Genetic variations of the apoE gene were detected using PCR and restriction fragment length polymorphism (RFLP).

RESULTSAn apoE gene mutation was identified in the patient's family. Sequence analysis confirmed a 9-bp deletion in the exon 4 of apoE gene from nt 484 to 492. The 9-bp deletion resulted in loss of 3 amino acids at positions 143-145. The sister of the propositus carried the same mutation, though she had neither proteinuria nor elevated plasma apoE. Sequence analysis of exon 3 showed no abnormality. No abnormalities were found in the father's apoE gene sequence. Analysis of genetic variations of the apoE gene by PCR and RFLP confirmed a 57 bp fragment consistent with the 9-bp deletion in exon 4. The father had a normal ε 3 ε 3 genotype.

CONCLUSIONThe 9 bp deletion of apoE may be associated with the pathogenesis of LPG.

Adolescent ; Apolipoproteins E ; blood ; genetics ; Exons ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Humans ; Kidney Diseases ; blood ; genetics ; Kidney Glomerulus ; metabolism ; pathology ; Lipoproteins ; blood ; Male ; Mutation ; Pedigree

Maintenance of healthy endothelium is essential to vascular homeostasis, and preservation of endothelial cell function is critical for transplant allograft function. Damage of microvascular endothelial cells is now regarded as a characteristic feature of acute vascular rejection and chronic allograft nephropathy, which is an important predictor of graft loss and is often associated with transplant vasculopathy. In this review, we will discuss the role of microvascular endothelium, in renal allograft dysfunction, particularly as it relates to markers of endothelial dysfunction and endothelial repair mechanisms. We also discuss the potential for therapies targeting endothelial dysfunction and transplant graft vasculopathy.
Humans ; Kidney/*blood supply ; *Kidney Transplantation ; Research Support, Non-U.S. Gov't ; Transplantation, Homologous ; Vascular Diseases/*prevention & control/*therapy