Proteinuria is a Prognostic Marker for Cardiovascular Mortality: NIPPON DATA 80, 1980-1999

Tanihara, Shinichi; Hayakawa, Takehito; Oki, Izumi; Nakamura, Yosikazu; Sakata, Kiyomi; Okayama, Akira; Fujita, Yasuyuki; Ueshima, Hirotsugu

doi:10.2188/jea.15.146

Cited by 21 publications

(37 citation statements)

References 27 publications

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“…14,15 Because the kidneys provide a significant route for clearance of methylarginines, 16,17 it is perhaps not surprising that ADMA 18 and SDMA concentrations increase in CKD patients even without proteinuria, 19,20 or that proteinuria with reduced renal function is associated with both elevated ADMA and endothelial dysfunction. 10,21,22 However, the patients in our study all had a nearly normal renal function. Inflammation, defined here as an elevated serum hsCRP, is also known to influence ADMA and has been proposed to be one factor linking ADMA to CVD.…”

Section: Discussionmentioning

confidence: 63%

ADMA Levels Correlate with Proteinuria, Secondary Amyloidosis, and Endothelial Dysfunction

Yılmaz¹,

Sönmez²,

Sağlam³

et al. 2008

Journal of the American Society of Nephrology

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Asymmetric dimethyl-arginine (ADMA), a residue of the proteolysis of arginine-methylated proteins, is a potent inhibitor of nitric oxide synthesis. The increased protein turnover that accompanies proteinuric secondary amyloidosis may increase circulating levels of ADMA, and this may contribute to endothelial dysfunction. We performed a cross-sectional study of 121 nondiabetic proteinuric patients with normal GFR (including 39 patients with nephrotic-range proteinuria and secondary amyloidosis) and 50 age-, sex-, and BMI-matched healthy controls. The proteinuric patients had higher levels of serum ADMA, symmetric dimethyl-arginine (SDMA), high-sensitivity C-reactive protein (hsCRP), and insulin resistance (homeostasis model assessment index) than controls. Compared with controls, brachial artery flow-mediated dilatation (FMD), serum L-Arginine, and the L-Arginine/ADMA ratio were significantly lower among proteinuric patients, suggesting greater endothelial dysfunction. When patients with secondary amyloidosis were compared with patients with glomerulonephritis who had similar levels of proteinuria, those with amyloidosis had higher ADMA and SDMA levels and lower L-Arginine/ADMA ratios and FMD measurements (P Ͻ 0.001 for all). Finally, even after adjusting for confounders, ADMA level correlated with both proteinuria and the presence of secondary amyloidosis, and was an independent predictor of FMD. We propose that ADMA synthesis may be increased in chronic kidney disease, especially in secondary amyloidosis, and this may explain part of the mechanism by which proteinuria increases cardiovascular morbidity and mortality.

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Section: Discussionmentioning

confidence: 63%

ADMA Levels Correlate with Proteinuria, Secondary Amyloidosis, and Endothelial Dysfunction

Yılmaz¹,

Sönmez²,

Sağlam³

et al. 2008

Journal of the American Society of Nephrology

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“…The small, but steady, percentage that continued to be exposed to immunosuppression over the observation period would suggest that this message needs to be emphasized. Again, although not proven by this study, conservative therapy including treatment of hypertension to lower BP targets (Ͻ130/80 mmHg) along with smoking cessation and treatment of hypercholesterolemia to LDL targets Ͻ2 mmol/L would seem prudent given the established risk factor of proteinuria in cardiovascular disease (23)(24)(25).…”

Section: Discussionmentioning

confidence: 79%

The Natural History of the Non-Nephrotic Membranous Nephropathy Patient

Hladunewich

Troyanov

Calafati

et al. 2009

Clinical Journal of the American Society of Nephrology

111

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Background and objectives: Although early studies suggest that patients with idiopathic membranous nephropathy (MGN) and subnephrotic range proteinuria overall do well, these studies were small and follow-up was short or difficult to discern.Design Conclusions: Patients with MGN and sustained subnephrotic range proteinuria have an excellent prognosis. Conservative management with close monitoring is recommended given the difficulty predicting which patients will develop nephrotic range proteinuria and then progress more rapidly.

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“…[31][32][33] Long-term trials have indicated an antiproteinuric effect of losartan. [33][34][35][36] In this study, the 3-month treatment with 100 mg losartan failed to show a significant UACR reduction in patients with morning hypertension (Figure 4a).…”

Section: Discussionmentioning

confidence: 99%

Losartan/hydrochlorothiazide combination vs. high-dose losartan in patients with morning hypertension—a prospective, randomized, open-labeled, parallel-group, multicenter trial

2012

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on behalf of the MAPPY Study InvestigatorsThe treatment of morning hypertension has not been established. We compared the efficacy and safety of a losartan/ hydrochlorothiazide (HCTZ) combination and high-dose losartan in patients with morning hypertension. A prospective, randomized, open-labeled, parallel-group, multicenter trial enrolled 216 treated outpatients with morning hypertension evaluated by home blood pressure (BP) self-measurement. Patients were randomly assigned to receive a combination therapy of 50 mg losartan and 12.5 mg HCTZ (n¼109) or a high-dose therapy with 100 mg losartan (n¼107), each of which were administered once every morning. Primary efficacy end points were morning systolic BP (SBP) level and target BP achievement rate after 3 months of treatment. At baseline, BP levels were similar between the two therapy groups. Morning SBP was reduced from 150.3 ± 10.1 to 131.5 ± 11.5 mm Hg by combination therapy (Po0.001) and from 151.0 ± 9.3 to 142.5 ± 13.6 mm Hg by high-dose therapy (Po0.001). The morning SBP reduction was greater in the combination therapy group than in the high-dose therapy group (Po0.001). Combination therapy decreased evening SBP from 141.6±13.3 to 125.3±13.1 mm Hg (Po0.001), and high-dose therapy decreased evening SBP from 138.9 ± 9.9 to 131.4 ± 13.2 mm Hg (Po0.01). Although both therapies improved target BP achievement rates in the morning and evening (Po0.001 for both), combination therapy increased the achievement rates more than high-dose therapy (Po0.001 and Po0.05, respectively). In clinic measurements, combination therapy was superior to high-dose therapy in reducing SBP and improving the achievement rate (Po0.001 and Po0.01, respectively). Combination therapy decreased urine albumin excretion (Po0.05) whereas high-dose therapy reduced serum uric acid. Both therapies indicated strong adherence and few adverse effects (Po0.001). In conclusion, losartan/HCTZ combination therapy was more effective for controlling morning hypertension and reducing urine albumin than high-dose losartan.

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Proteinuria is a Prognostic Marker for Cardiovascular Mortality: NIPPON DATA 80, 1980-1999

Cited by 21 publications

References 27 publications

ADMA Levels Correlate with Proteinuria, Secondary Amyloidosis, and Endothelial Dysfunction

ADMA Levels Correlate with Proteinuria, Secondary Amyloidosis, and Endothelial Dysfunction

The Natural History of the Non-Nephrotic Membranous Nephropathy Patient

Losartan/hydrochlorothiazide combination vs. high-dose losartan in patients with morning hypertension—a prospective, randomized, open-labeled, parallel-group, multicenter trial

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