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Ng CF et al, 2018: Extracorporeal Shockwave Lithotripsy Could Lead to a Prolonged Increase in the Renal Fibrotic Process of Up to 2 Years.

Ng CF, Luke S, Yee CH, Leung SCH, Teoh JYC, Yuen J.
SH Ho Urology Centre, Department of Surgery, The Chinese University of Hong Kong, Shatin, Hong Kong .
School of Nursing, Hong Kong Polytechnic University , Hung Hom, Hong Kong.

Abstract

INTRODUCTION AND OBJECTIVE: This prospective study aimed to evaluate the effect of ramping and pause protocols on renal fibrosis, blood pressure control, and renal function in patients receiving extracorporeal shockwave lithotripsy (SWL).
PATIENTS AND METHODS: This study prospectively recruited 320 patients with solitary radiopaque renal stones <15 mm in size. Patients were randomized to receive one of four shockwave protocols: (1) standard protocol (no ramping or pause); (2) ramping protocol alone; (3) ramping and pause protocols; or (4) pause protocol alone. Spot urine samples were collected before and for 2 years after treatment to monitor the levels of the renal fibrosis marker procollagen III aminoterminal propeptide (PIIINP) by blinded research staffs. Blood pressure and serum creatinine levels were also monitored during follow-up.
RESULTS: The four groups had comparable baseline data and treatment parameters. Significant increases (p < 0.05) in the urinary PIIINP levels from 6 weeks until 18 months after SWL were observed among all patients and in individual groups. PIIINP levels peaked at 1 year after SWL and gradually decreased to the baseline at 2 years. At the 2-year follow-up point, the overall serum creatinine levels remained significantly elevated (76.21-80.01 μmol/L, p < 0.001). Twenty (9.95%) patients developed new-onset hypertension and another 43 (36.4%) experienced worsening blood pressure control. However, no differences were observed among the four treatment groups.
CONCLUSIONS: SWL led to significant increases in renal fibrosis marker levels for up to 18 months after treatment. However, no differences in changes in renal fibrosis marker and serum creatinine levels and worsening of blood pressure control were observed with respect to the use of either ramping or pause treatment protocols.

J Endourol. 2018 Jan 9. doi: 10.1089/end.2017.0684. [Epub ahead of print]

 

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Comments 1

Peter Alken on Friday, 06 July 2018 12:13

A carefully selected title for a paper with alarming specifications:
“In the literature, the average annual incidence of add-on pharmacotherapy among local hypertensive patients was 4.71% to 6.41%. Therefore, our add-on therapy rate of 36.4% during the 2-year follow-up was much higher than that in the general population.” In addition the serum creatinine levels were significantly elevated and the renal fibrosis marker PIIINP was above pre-ESWL values during nearly two years. This marker was first described in 1997
(Urinary and serum type III collagen: markers of renal fibrosis. Soylemezoglu O et al. Nephrol Dial Transplant. 1997 Sep;12(9):1883-9). But its career does not seem to have been very successful. A recent review on biomarkers for the detection of renal fibrosis (Biomarkers for the detection of renal fibrosis and prediction of renal outcomes: a systematic review. Mansour SG et al. BMC Nephrol. 2017 Feb 20;18(1):72) emphasized the need of these markers: “It is important to identify and predict renal fibrosis via the use of biomarkers since tubulointerstitial fibrosis is the unifying feature in progressive renal disease irrespective of the initial insult.”
With only 3 studies matching the selection criteria in 20 years PIIINP did not make it into the small number of 3 markers “TGF-β, MCP-1 and MMP-2 which may identify patients at risk for renal fibrosis and hence worse renal outcomes.” The authors’ statement of the present paper seems to be too optimistic: “PIIINP is an advantageous marker of renal fibrosis because its measurement is simple and convenient, and it can provide an overall view of fibrosis in the whole kidney after SWL. Therefore,we used PIIINP to quantitatively assess renal fibrosis afterSWL in our cohort.” We will see more publications on this marker.

A carefully selected title for a paper with alarming specifications: “In the literature, the average annual incidence of add-on pharmacotherapy among local hypertensive patients was 4.71% to 6.41%. Therefore, our add-on therapy rate of 36.4% during the 2-year follow-up was much higher than that in the general population.” In addition the serum creatinine levels were significantly elevated and the renal fibrosis marker PIIINP was above pre-ESWL values during nearly two years. This marker was first described in 1997 (Urinary and serum type III collagen: markers of renal fibrosis. Soylemezoglu O et al. Nephrol Dial Transplant. 1997 Sep;12(9):1883-9). But its career does not seem to have been very successful. A recent review on biomarkers for the detection of renal fibrosis (Biomarkers for the detection of renal fibrosis and prediction of renal outcomes: a systematic review. Mansour SG et al. BMC Nephrol. 2017 Feb 20;18(1):72) emphasized the need of these markers: “It is important to identify and predict renal fibrosis via the use of biomarkers since tubulointerstitial fibrosis is the unifying feature in progressive renal disease irrespective of the initial insult.” With only 3 studies matching the selection criteria in 20 years PIIINP did not make it into the small number of 3 markers “TGF-β, MCP-1 and MMP-2 which may identify patients at risk for renal fibrosis and hence worse renal outcomes.” The authors’ statement of the present paper seems to be too optimistic: “PIIINP is an advantageous marker of renal fibrosis because its measurement is simple and convenient, and it can provide an overall view of fibrosis in the whole kidney after SWL. Therefore,we used PIIINP to quantitatively assess renal fibrosis afterSWL in our cohort.” We will see more publications on this marker.
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