letter to the editor
http://www.kidney-international.org & 2015 International Society of Nephrology
Regarding ‘Long-term risks for kidney donors’ To the Editor: In contrast to previous studies, Mjoen et al.1 found that ‘kidney donors are at increased long-term risk for ESRD, cardiovascular, and all-cause mortality compared with a control group of non-donors who would have been eligible for donation’. The authors argue that inconsistency with earlier studies is explained by the use of inappropriate control groups (i.e., the general population) or inadequate follow-up. However, the authors do not discuss long-term follow-up studies of patients who underwent nephrectomy for other reasons, a situation that is not confounded by superior health of the index subjects. In 1968, Andersen et al.2 reported that survival following uninephrectomy for a benign renal condition was the same as that of the general population if the remaining kidney were normal. Narkun-Burgess et al.3 reported that, after 45 years, survival among World War II (WW II) veterans who lost a kidney due to trauma was similar to the matched control WW II veterans and Robitaille et al.4 found little evidence of renal damage among people who had undergone uninephrectomy in childhood after a mean follow-up of 23 years. Given the known geographic variations in health status,5 is it possible that in Mjoen’s study, people living in the control county (NordTrondelag) were healthier than the entire Norwegian population that supplied the kidney donors? If so, this could explain the seemingly contradictory results. 1. 2. 3. 4.
5.
Mjoen G, Hallan S, Hartmann A et al. Long-term risks for kidney donors. Kidney Int 2014; 86: 162–167. Andersen B, Hansen JB, Jorgensen SJ. Survival after nephrectomy. Scand J Urol Nephrol 1968; 2: 91–94. Narkun-Burgess DM, Nolan CR, Norman JE et al. Forty-five year follow-up after uninephrectomy. Kidney Int 1993; 43: 1110–1115. Robitaille P, Lortie L, Mongeau JG, Sinnassamy P. Long-term follow-up of patients who underwent unilateral nephrectomy in childhood. Lancet 1985; 325: 1297–1299. Salmela R. Regional inequalities in health and health care in Finland and Norway. Health Policy 1993; 24: 83–94.
Aaron Spital1 1
Mount Sinai St Luke’s, New York, New York, USA Correspondence: Aaron Spital, Mount Sinai St Luke’s, Department of Nephrology, Amsterdam Avenue, New York, NY 10025, USA. E-mail: [email protected] Kidney International (2015) 87, 660; doi:10.1038/ki.2014.397
The Authors Reply: We would like to thank Dr Spital1 for his interest in our paper.2 First, he wonders why we did not discuss studies on nephrectomy for other causes, as these could perhaps be less confounded by superior health of the index person. The studies mentioned1 included few individuals, 173, 28, and 13. They were published at a time when no long-term donor data were available. When discussing healthy kidney donors in the current era these 660
studies are less relevant. In our opinion, the only relevant comparison for healthy donors is healthy controls. Second, he wonders whether people living in the single county where the HUNT study was conducted, from which the control group was drawn from, were healthier compared with the Norwegian population. We acknowledged in our paper that regional differences might be a potential limitation. The HUNT study, from which the controls were drawn, is regarded as fairly representative of Norway. Moreover, it is important to note that the selection process per se might favor donors as they undergo additional extensive medical examinations. 1. 2.
Spital A. Regarding ‘Long-term risks for kidney donors’. Kidney Int 2015; 87: 660. Mj en G, Hallan S, Hartmann A et al. Long-term risks for kidney donors. Kidney Int 2014; 86: 162–167.
Geir Mj en1 and Hallvard Holdaas2 1
Department of Medicine, Oslo University Hospital, Oslo, Norway and Department of Transplant Medicine, Oslo University Hospital, Oslo, Norway Correspondence: Geir Mjoen, Department of Medicine, Oslo University Hospital, Kirkeveien, Oslo 0027, Norway. E-mail: [email protected] 2
Kidney International (2015) 87, 660; doi:10.1038/ki.2014.400
Incretin-based drugs and renoprotection—is hyperfiltration key? To the Editor: With interest we read the review by Tanaka et al., summarizing the potential renoprotective properties of incretin-based drugs in diabetic kidney disease (DKD). The review focuses on the effects beyond glucose lowering of incretin-based therapies on several factors involved in the pathogenesis of DKD.1 Although the authors mention glomerular hypertension, which may clinically present as hyperfiltration, as a causal feature in DKD development, they do not discuss the promising potential of incretin-based therapies to ameliorate this classical risk factor. Indeed, glucagon-like peptide-1 (GLP-1) receptor agonists reduce hyperfiltration in rodents with diabetes.2 In obese hyperfiltrating males, 25% of whom had type 2 diabetes, GLP-1 infusion decreased the glomerular filtration rate (GFR).3 Several mechanisms are proposed to explain the beneficial actions on renal hemodynamics and hyperfiltration. Obesity and diabetes-associated proximal sodium hyperreabsorption result in reduced sodium delivery at the distally located macula densa, leading to afferent vasodilation and increased glomerular pressure via tubuloglomerular feedback.2,3 GLP-1 decreases proximal sodium reabsorption by inhibiting the sodium–hydrogen exchanger-3, thereby potentially restoring this maladaptive response.2,3 Alternatively, GLP-1 and associated therapies may decrease hyperfiltration by direct actions on the renal vasculature or through effects on vasoactive factors.2 Importantly, in healthy normofiltrating Kidney International (2015) 87, 660–664
http://www.kidney-international.org & 2015 International Society of Nephrology
Regarding ‘Long-term risks for kidney donors’ To the Editor: In contrast to previous studies, Mjoen et al.1 found that ‘kidney donors are at increased long-term risk for ESRD, cardiovascular, and all-cause mortality compared with a control group of non-donors who would have been eligible for donation’. The authors argue that inconsistency with earlier studies is explained by the use of inappropriate control groups (i.e., the general population) or inadequate follow-up. However, the authors do not discuss long-term follow-up studies of patients who underwent nephrectomy for other reasons, a situation that is not confounded by superior health of the index subjects. In 1968, Andersen et al.2 reported that survival following uninephrectomy for a benign renal condition was the same as that of the general population if the remaining kidney were normal. Narkun-Burgess et al.3 reported that, after 45 years, survival among World War II (WW II) veterans who lost a kidney due to trauma was similar to the matched control WW II veterans and Robitaille et al.4 found little evidence of renal damage among people who had undergone uninephrectomy in childhood after a mean follow-up of 23 years. Given the known geographic variations in health status,5 is it possible that in Mjoen’s study, people living in the control county (NordTrondelag) were healthier than the entire Norwegian population that supplied the kidney donors? If so, this could explain the seemingly contradictory results. 1. 2. 3. 4.
5.
Mjoen G, Hallan S, Hartmann A et al. Long-term risks for kidney donors. Kidney Int 2014; 86: 162–167. Andersen B, Hansen JB, Jorgensen SJ. Survival after nephrectomy. Scand J Urol Nephrol 1968; 2: 91–94. Narkun-Burgess DM, Nolan CR, Norman JE et al. Forty-five year follow-up after uninephrectomy. Kidney Int 1993; 43: 1110–1115. Robitaille P, Lortie L, Mongeau JG, Sinnassamy P. Long-term follow-up of patients who underwent unilateral nephrectomy in childhood. Lancet 1985; 325: 1297–1299. Salmela R. Regional inequalities in health and health care in Finland and Norway. Health Policy 1993; 24: 83–94.
Aaron Spital1 1
Mount Sinai St Luke’s, New York, New York, USA Correspondence: Aaron Spital, Mount Sinai St Luke’s, Department of Nephrology, Amsterdam Avenue, New York, NY 10025, USA. E-mail: [email protected] Kidney International (2015) 87, 660; doi:10.1038/ki.2014.397
The Authors Reply: We would like to thank Dr Spital1 for his interest in our paper.2 First, he wonders why we did not discuss studies on nephrectomy for other causes, as these could perhaps be less confounded by superior health of the index person. The studies mentioned1 included few individuals, 173, 28, and 13. They were published at a time when no long-term donor data were available. When discussing healthy kidney donors in the current era these 660
studies are less relevant. In our opinion, the only relevant comparison for healthy donors is healthy controls. Second, he wonders whether people living in the single county where the HUNT study was conducted, from which the control group was drawn from, were healthier compared with the Norwegian population. We acknowledged in our paper that regional differences might be a potential limitation. The HUNT study, from which the controls were drawn, is regarded as fairly representative of Norway. Moreover, it is important to note that the selection process per se might favor donors as they undergo additional extensive medical examinations. 1. 2.
Spital A. Regarding ‘Long-term risks for kidney donors’. Kidney Int 2015; 87: 660. Mj en G, Hallan S, Hartmann A et al. Long-term risks for kidney donors. Kidney Int 2014; 86: 162–167.
Geir Mj en1 and Hallvard Holdaas2 1
Department of Medicine, Oslo University Hospital, Oslo, Norway and Department of Transplant Medicine, Oslo University Hospital, Oslo, Norway Correspondence: Geir Mjoen, Department of Medicine, Oslo University Hospital, Kirkeveien, Oslo 0027, Norway. E-mail: [email protected] 2
Kidney International (2015) 87, 660; doi:10.1038/ki.2014.400
Incretin-based drugs and renoprotection—is hyperfiltration key? To the Editor: With interest we read the review by Tanaka et al., summarizing the potential renoprotective properties of incretin-based drugs in diabetic kidney disease (DKD). The review focuses on the effects beyond glucose lowering of incretin-based therapies on several factors involved in the pathogenesis of DKD.1 Although the authors mention glomerular hypertension, which may clinically present as hyperfiltration, as a causal feature in DKD development, they do not discuss the promising potential of incretin-based therapies to ameliorate this classical risk factor. Indeed, glucagon-like peptide-1 (GLP-1) receptor agonists reduce hyperfiltration in rodents with diabetes.2 In obese hyperfiltrating males, 25% of whom had type 2 diabetes, GLP-1 infusion decreased the glomerular filtration rate (GFR).3 Several mechanisms are proposed to explain the beneficial actions on renal hemodynamics and hyperfiltration. Obesity and diabetes-associated proximal sodium hyperreabsorption result in reduced sodium delivery at the distally located macula densa, leading to afferent vasodilation and increased glomerular pressure via tubuloglomerular feedback.2,3 GLP-1 decreases proximal sodium reabsorption by inhibiting the sodium–hydrogen exchanger-3, thereby potentially restoring this maladaptive response.2,3 Alternatively, GLP-1 and associated therapies may decrease hyperfiltration by direct actions on the renal vasculature or through effects on vasoactive factors.2 Importantly, in healthy normofiltrating Kidney International (2015) 87, 660–664
