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. 2015 Apr 7;17(8):656. doi: 10.1111/jch.12543

Reply to: Hemodynamic and Arterial Stiffness Parameters in Ambulatory Blood Pressure Phenotypes and the Clinical Scenario of Polypharmacy and Comorbidities

Baris Afsar 1, Mehmet Kanbay 2
PMCID: PMC8031649  PMID: 25857208

We thank Dr Anyfanti and colleagues1 for their interest in our paper. They raised some important questions regarding our manuscript. First, the authors suggest that our patient population had high urinary albumin excretion (UAE) and urinary protein excretion (UPE) values and low creatinine clearance.1 Indeed, this is one of the important aspects of our study. We recruited patients who attended a nephrology clinic and who were mostly consulted from other clinics for suspected or known kidney disease. Thus, it is not surprising that these patients had high UAE and UPE values and low creatinine clearance. Instead of examining patients in idealized laboratory conditions, we examined patients in routine daily practice in an attempt to understand what clinic nephrologists face every day. This is the reason we included patients with chronic kidney disease (CKD) and diabetes and those using various medications.

Second, the authors suggest providing UAE and UPE according to the stages of CKD and the presence of diabetes.

Another important issue is the definition of CKD itself. Classically, CKD was based on creatinine clearance; however, recent evidence suggests that increased albumin/protein excretion is also a marker of CKD, illustrated by the fact that one person may have CKD without decreased glomerular filtration rate. Based on these issues, we performed separate analyses in diabetic and nondiabetic patients, the results of which are given in the Table according to stage of CKD.

Table 1.

Comparison of Urinary Albumin and Urinary Protein Excretion Among Patients With and Without Diabetes

Diabetes Mellitus (+) (n=86) Diabetes Mellitus (−) (n=124) P Valuea
Urinary albumin excretion, mg/d 578.3±1418.2 255.8±622.6 .071
Urinary protein excretion, mg/d 956.3±1998.6 511.2±902.2 .445
a

P value is based on Mann‐Whitney U test.

The mean UPE values were 349, 317, 934, 2495, and 2200 mg/d in stage 1, stage 2, stage 3, stage 4, and stage 5 CKD patients, respectively. The mean UAE values were 111, 119, 610, 1616, and 1215 mg/d in stage 1, stage 2, stage 3, stage 4, and stage 5 CKD patients, respectively.

Third, the authors warned that the distribution of UAE and UPE is not normal and the values should be given as median and interquartile ranges. However, this is not a must. The median and interquartile ranges for UAE were 25.2 (14.1–154.3) and for UPE were 213 (138.5–440.5), respectively.

Fourth, the authors wondered whether the patients with resistant hypertension differed with respect to dipping profiles and hypertension subtypes.

There were 17 patients with resistant hypertension (defined as a blood pressure that remains ≥140 mm Hg and/or 90 mm Hg despite therapy with three or more full‐dose antihypertensive drugs). Among these patients, three had white‐coat hypertension, one had masked hypertension, and 13 had sustained hypertension (P<.0001). The distribution of patients with resistant hypertension regarding the dipping profile was as follows: two were normal dippers, two were extreme dippers, seven were nondippers, and six were reverse dippers (P=.021).

Fifth, the authors suggest that the explanation for the worse prognosis in extreme dippers cannot be explained in terms of increased sympathetic activation and renin‐angiotensin system as a result of drug treatment. We agree with this; however, our suggestion is based on previous data. We can make only a hypothesis at this point. As we suggest in the original manuscript, these can be tested in patients with pure hypertension without any treatment, although it is difficult.

Lastly, we used the terms sustained hypertension, white‐coat hypertension, masked hypertension, and sustained normotension based on previous definitions. The suggestions of the authors may be true in logic; however, to the best of our knowledge, there is no distinction while defining these terms (whether on antihypertensive medication or not).

Again, we thank Dr Anyfanti and colleagues for their interest in our paper.

References

  • 1. Anyfanti P, Triantafyllou A, Douma S. Hemodynamic and arterial stiffness parameters in ambulatory blood pressure phenotypes and the clinical scenario of polypharmacy and comorbidities. J Clin Hypertens (Greenwich). 2015;17:655. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2. Afsar B, Elsurer R, Kirkpantur A, Kanbay M. Urinary sodium excretion and ambulatory blood pressure findings in patients with hypertension. J Clin Hypertens (Greenwich). 2015;17:200–206. [DOI] [PMC free article] [PubMed] [Google Scholar]

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