Impact of elevated intact parathyroid hormone on mortality and renal disease progression in patients with chronic kidney disease stages 3 and 4

2012 ◽  
Vol 28 (9) ◽  
pp. 1527-1536 ◽  
Author(s):  
C.V. Asche ◽  
S.E. Marx ◽  
J. Kim ◽  
S.K. Unni ◽  
D. Andress
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Intact Parathyroid Hormone ◽  
Renal Disease Progression ◽  
Disease Stages

scholarly journals Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Reciprocal Relationship ◽  
Current Evidence ◽  
Renal Disease Progression ◽  
Lowering Therapy ◽  
The Relationship

The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

Effect of Urate Lowering Therapy on Renal Disease Progression in Hyperuricemic Patients with Chronic Kidney Disease

2015 ◽  
Vol 42 (11) ◽  
pp. 2143-2148 ◽  
Author(s):  
Yoonjin Kim ◽  
Sungjoon Shin ◽  
Kyungsoo Kim ◽  
Sangtae Choi ◽  
Kwanghoon Lee
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Serum Uric Acid ◽  
Serum Uric Acid Level ◽  
Renal Disease Progression ◽  
Time Curve ◽  
Lowering Therapy

Objective.To determine whether urate lowering therapy (ULT) could delay renal disease progression in hyperuricemic patients with chronic kidney disease (CKD).Methods.We performed a retrospective review of hyperuricemic patients with stage 3 CKD followed from September 2005 to July 2014 in Dongguk University Ilsan Hospital, Goyang, Korea. A total of 158 eligible patients were identified and 65 of them were treated with ULT in addition to the usual CKD management. We divided the patients according to the use of ULT and compared the estimated glomerular filtration rate (eGFR) change from baseline value and the proportion of renal disease progression (decline of eGFR > 30% of the baseline value, initiation of dialysis or eGFR < 15 ml/min/1.73m2) at the time of last followup. Risk factors for renal disease progression were identified by logistic regression analysis.Results.After a median followup of 118.5 weeks (minimum 25, maximum 465), the ULT group showed better outcomes compared to the non-ULT group in terms of eGFR change from baseline (−1.19 ± 12.07 vs −7.37 ± 11.17 ml/min/1.73 m2, p = 0.001) and the proportion of renal disease progression (12.3% vs 27.9%, p = 0.01). Goal-directed ULT showed better clinical outcomes compared to maintaining the initial ULT dose. Actual (area under the SUA-time curve adjusted by total observation time period) serum uric acid was significantly associated with the risk of renal disease progression (p for trend = 0.04) and actual serum uric acid level < 7 mg/dl reduced the risk of renal disease progression by 69.4%.Conclusion.ULT significantly delayed renal disease progression in hyperuricemic patients with CKD. Goal-directed ULT seems to be better than continuing the initial ULT prescription.

scholarly journals Cystatin C as a Predictor of Mortality and Cardiovascular Events in a Population with Chronic Kidney Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Ana Vigil ◽  
Emilia Condés ◽  
Luis Vigil ◽  
Paloma Gallar ◽  
Aniana Oliet ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Cystatin C ◽  
Cardiovascular Events ◽  
Interquartile Range ◽  
Renal Disease Progression ◽  
The Third ◽  
Overall Mortality

Background. We examine whether cystatin C, a surrogate marker of renal function, could identify patients with chronic kidney disease (CKD) with an increased risk of renal disease progression, death, or cardiovascular events.Methods. Data were obtained for 180 patients, with a diagnosis of chronic renal failure based on serum creatinine estimated glomerular filtration rate (eGFRcreat) <90 mL/min/1.73 m2. This population was grouped in tertiles according to cystatin C and creatinine values at baseline. Cardiovascular events and overall mortality were estimated for each tertile. Predictors of overall mortality and for the development of renal disease progression were analyzed.Results. The median age was 75 years (interquartile range 69–82) and the median eGFRcreat38 mL/min m2(interquartile range 33–49). Overall mortality was lower on the first and on the second tertiles of cystatin C than on the third one (HR = 0.060; 95% CI: 0.008–0.447 and HR = 0.094; 95% CI: 0.022–0.406, resp.). Deaths related to the creatinine tertiles followed the same pattern, but differences were not as large. Cardiovascular mortality was lower on the second than on the third cystatin C tertile (HR = 0.198; 95% CI: 0.040–0.987), but it did not show differences on the first and the second creatinine tertiles compared with the third one (HR = 0.126; 95% CI: 0.013–1.265 and HR = 0.403; 95% CI: 0.093–1.740). The only independent predictors of mortality during followup were baseline cystatin C (OR = 0.100; 95% CI: 0.021–0.463) and baseline uric acid (OR = 1.377; 95% CI: 1.070–1.773).Conclusion. Cystatin C may be an alternative to creatinine for detecting a high risk of death and cardiovascular events in a population with CKD.

scholarly journals The Severity of Diabetic Retinopathy Is an Independent Factor for the Progression of Diabetic Nephropathy

2020 ◽  
Vol 10 (1) ◽  
pp. 3
Author(s):  
Shi-Chue Hsing ◽  
Chia-Cheng Lee ◽  
Chin Lin ◽  
Jiann-Torng Chen ◽  
Yi-Hao Chen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Retinopathy ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Renal Disease Progression ◽  
Hazard Ratios ◽  
Stage Renal Disease ◽  
End Stage

(1) Background: It has rarely been studied whether the severity of diabetic retinopathy (DR) could influence renal disease progression in end-stage renal disease (ESRD) and chronic kidney disease (CKD) in patients with type 2 diabetes. The aim of this study was to evaluate renal disease progression in ESRD and CKD according to DR severity in patients with type 2 diabetes. (2) Methods: We included 1329 patients and divided the cohort into two end-points. The first was to trace the incidence of ESRD in all enrolled participants and the other was to follow their progression to CKD. (3) Results: Significantly higher crude hazard ratios (HRs) of ESRD incidence in all enrolled participants were noted, and this ratio increased in a stepwise fashion. However, after adjustment, DR severity was not associated with ESRD events. Therefore, a subgroup of 841 patients without CKD was enrolled to track their progression to CKD. Compared with no diabetic retinopathy, the progression of CKD increased in a stepwise fashion, from mild nonproliferative diabetic retinopathy (NPDR) to moderate NPDR, to severe NPDR and to proliferative diabetic retinopathy (PDR), both in the crude and adjusted models. (4) Conclusions: The severity of retinopathy appeared to be associated with renal lesions and the development of CKD. Our findings suggest that the severity of DR is a risk factor for progression to CKD. Therefore, diabetic retinopathy is useful for prognosticating the clinical course of diabetic kidney disease.

scholarly journals Serum intact parathyroid hormone levels in cats with chronic kidney disease

2013 ◽  
Vol 33 (2) ◽  
pp. 229-235 ◽  
Author(s):  
Luciano H. Giovaninni ◽  
Marcia M. Kogika ◽  
Marcio D. Lustoza ◽  
Archivaldo Reche Junior ◽  
Vera A.B.F. Wirthl ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Stage Iv ◽  
Control Group ◽  
Intact Parathyroid Hormone ◽  
Acid Base ◽  
Acid Base Status ◽  
Serum Ionized Calcium ◽  
Progression Of Renal Disease

Chronic kidney disease (CKD) is frequently observed in cats and it is characterized as a multisystemic illness, caused by several underlying metabolic changes, and secondary renal hyperparathyroidism (SRHPT) is relatively common; usually it is associated with the progression of renal disease and poor prognosis. This study aimed at determining the frequency of SRHPT, and discussing possible mechanisms that could contribute to the development of SRHPT in cats at different stages of CKD through the evaluation of calcium and phosphorus metabolism, as well as acid-base status. Forty owned cats with CKD were included and divided into three groups, according to the stages of the disease, classified according to the International Renal Interest Society (IRIS) as Stage II (n=12), Stage III (n=22) and Stage IV (n=6). Control group was composed of 21 clinically healthy cats. Increased serum intact parathyroid hormone (iPTH) concentrations were observed in most CKD cats in all stages, and mainly in Stage IV, which hyperphosphatemia and ionized hypocalcemia were detected and associated to the cause for the development of SRHPT. In Stages II and III, however, ionized hypercalcemia was noticed suggesting that the development of SRHPT might be associated with other factors, and metabolic acidosis could be involved to the increase of serum ionized calcium. Therefore, causes for the development of SRHPT seem to be multifactorial and they must be further investigated, mainly in the early stages of CKD in cats, as hyperphosphatemia and ionized hypocalcemia could not be the only factors involved.

Renal disease

2011 ◽  
pp. 631-656
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Nephrotic Syndrome ◽  
Kidney Disease ◽  
Renal Disease ◽  
Nutritional Assessment ◽  
Kidney Injury ◽  
Nutritional Requirements ◽  
P Nutrition ◽  
Disease Stages

Introduction 632 Nutritional assessment 634 Malnutrition in renal disease 636 Nutritional considerations in chronic kidney disease 638 Nutrition in acute kidney injury 641 Nutrition in chronic kidney disease stages 3 and 4 642 Nephrotic syndrome 644 Nutritional requirements in dialysis 646 Nutritional requirements in haemodialysis ...

scholarly journals Outcome of supplementation of vitamin D on intact parathyroid hormone level in chronic kidney disease patients

2019 ◽  
Vol 8 (2) ◽  
pp. 51-54
Author(s):  
Laxman Prasad Adhikary ◽  
Aarjan Khanal
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Hormone Level ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Intact Parathyroid Hormone ◽  
Parathyroid Hormone Level ◽  
Modifiable Factors ◽  
The Mean

Background: Secondary hyperparathyroidism is present in majority of patients with estimated glomerular filtrate rate less than 60 mL/min/1.73 m2. Sustained elevated parathyroid hormone level can cause osteitis-fibrosa-cystica, fracture, hypercalcemia, hyperphosphatemia, and calciphylaxis. Kidney Disease Improving Global Outcome guidelines for Chronic Kidney Disease Mineral and Bone Disorder 2017 recommends treatment with calcitriol or vitamin D analogue if parathyroid hormone level is progressively increasing and remains persistently above the upper limit despite correction of modifiable factors. Objectives: The objective of this study was to determine the mean change in intact parathyroid hormone aftercalcitriol supplementation in patients with chronic kidney disease (stage 3 to 5). Methodology: This prospective observational study enrolled 92 patients with chronic kidney disease stage 3 to 5, not under maintenance hemodialysis. Patients who had intact parathyroid hormone level more than 200 pg/ml, serum phosphate level less than 4.5 mg/dl and corrected serum calcium less than 9.5 mg/dl were selected for the study. They were supplemented with oral calcitriol 0.25μg thrice weekly for three months and intact parathyroid hormone level was measured after three months. Results: Mean intact parathyroid hormone level before supplementation was 332.91 ± 96.046pg/ml and after three months of supplementation with calcitriol was 176.49 ±53.764pg/ml. This finding was statistically significant (Correlation: 0.471, p-value less than 0.05). Thus, supplementation of calcitriol reduced the mean intact parathyroid hormone level in the chronic kidney disease patients in our study. Conclusion: Calcitriol supplementation seems to be an effective measure to reduce intact parathyroid hormone level in chronic kidney disease patients when it remains persistently high despite correction of modifiable factors.

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