Kidney Hyperfiltration After Nephrectomy: A Mechanism to Restore Kidney Function in Living Donors
Living donor kidney transplantation (LDKT) is the treatment of choice for patients with end stage renal disease (ESRD). Up to now, the studies reporting the impact of nephrectomy in living kidney donors to their future kidney function were limited. Most living donors undergo recovery of kidney function after nephrectomy owing to remnant kidneys’ capability to compensate nephron loss through adaptive hyperfiltration. However, hyperfiltration may fail and turn out to be maladaptive, causing deterioration of donors’ kidney function and increasing risk of chronic kidney disease (CKD) in long term. Hyperfiltration is caused by increased in kidney blood flow and glomerular hypertrophy. Both conditions are regulated by various factors. The adaptive hyperfiltration in the early phase after nephrectomy may play important role in determining long term kidney function, but factors affecting the process are still unclear. Hyperfiltration may also be influenced by donors’ characteristics such as age, body mass index (BMI), family related to the recipient, arterial stiffness and intraoperative intrabdominal pressure. Further study to understand the mechanism of hyperfiltration is needed so that kidney transplant centers could anticipate its failure and the detrimental effects of nephrectomy in the future.
Choi K, Yang S, Joo D, et al., editors. Clinical assessment of renal function stabilization after living donor nephrectomy. Transplantation proceedings. Elsevier; 2012.
Tonelli M, Wiebe N, Knoll G, et al. Systematic review: kidney transplantation compared with dialysis in clinically relevant outcomes. 2011;11(10):2093-109.
Mueller TF, Luyckx VAJJotASoN. The natural history of residual renal function in transplant donors. 2012;23(9):1462-6.
Lenihan CR, Busque S, Derby G, Blouch K, Myers BD, Tan JC. Longitudinal study of living kidney donor glomerular dynamics after nephrectomy. J Clin Invest. 2015;125(3):1311-8.
Srivastava T, Celsi GE, Sharma M, et al. Fluid flow shear stress over podocytes is increased in the solitary kidney. 2014;29(1):65-72.
Chen Z, Fang J, Li G, et al., editors. Compensatory changes in the retained kidney after nephrectomy in a living related donor. Transplantation proceedings. Elsevier; 2012.
Kwon H, Kim D, Jang H, et al., editors. Predictive factors of renal adaptation after nephrectomy in kidney donors. Transplantation proceedings. Elsevier; 2017.
Muzaale AD, Massie AB, Wang M-C, et al. Risk of end-stage renal disease following live kidney donation. 2014;311(6):579-86.
Fesler P, Mourad G, Du Cailar G, Ribstein J, Mimran AJAJoP-RP. Arterial stiffness: an independent determinant of adaptive glomerular hyperfiltration after kidney donation. 2015;308(6):F567-F71.
Nogueira JM, Weir MR, Jacobs S, Breault D, Klassen D, Evans DA, et al. A study of renal outcomes in obese living kidney donors. 2010;90(9):993-9.
Jeon HG, Lee SR, Joo DJ, Oh YT, Kim MS, Kim YS, et al. Predictors of kidney volume change and delayed kidney function recovery after donor nephrectomy. 2010;184(3):1057-63.
Kuppe C, Rohlfs W, Grepl M, Schulte K, Veron D, Elger M, et al. Inverse correlation between vascular endothelial growth factor back-filtration and capillary filtration pressures. 2018;33(9):1514-25.
Sigmon DH, Gonzalez-Feldman E, Cavasin MA, D’Anna LP, Beierwaltes WHJJotASoN. Role of nitric oxide in the renal hemodynamic response to unilateral nephrectomy. 2004;15(6):1413-20.
Chatauret N, Badet L, Barrou B, Hauet TJPeu. Ischemia-reperfusion: From cell biology to acute kidney injury. 2014;24:S4-S12.
Gengrinovitch S, Berman B, David G, Witte L, Neufeld G, Ron DJJoBC. Glypican-1 is a VEGF165 binding proteoglycan that acts as an extracellular chaperone for VEGF165. 1999;274(16):10816-22.
Schrijvers BF, Flyvbjerg A, Tilton RG, Rasch R, Lameire NH, De Vriese ASJNEn. Pathophysiological role of vascular endothelial growth factor in the remnant kidney. 2005;101(1):e9-e15.
Wu H, Chen G, Wyburn KR, Yin J, Bertolino P, Eris JM, et al. TLR4 activation mediates kidney ischemia/reperfusion injury. 2007;117(10):2847-59.
Ma Y, Yabluchanskiy A, Lindsey MLJF, repair t. Neutrophil roles in left ventricular remodeling following myocardial infarction. 2013;6(1):11.
Denic A, Mathew J, Lerman LO, Lieske JC, Larson JJ, Alexander MP, et al. Single-nephron glomerular filtration rate in healthy adults. 2017;376(24):2349-57.
Toyoda M, Yamanaga S, Kawabata C, et al., editors. Long-term safety of living kidney donors aged 60 and older. Transplantation proceedings. Elsevier; 2014.
Suneja M, Kumar ABJJocc. Obesity and perioperative acute kidney injury: a focused review. 2014;29(4):694. e1-e6.
Mascali A, Franzese O, Nistico S, et al. Obesity and kidney disease: Beyond the hyperfiltration. London, England: SAGE Publications; 2016.
Skrunes R, Svarstad E, Reisæter AV, Vikse BEJCJotASoN. Familial clustering of ESRD in the Norwegian population. 2014;9(10):1692-700.
Mjøen G, Hallan S, Hartmann A, et al. Long-term risks for kidney donors. 2014;86(1):162-7.
Elsherbiny HE, Alexander MP, Kremers WK, et al. Nephron hypertrophy and glomerulosclerosis and their association with kidney function and risk factors among living kidney donors. 2014;9(11):1892-902.
I Georgianos P, A Sarafidis P, N Lasaridis AJCvp. Arterial stiffness: a novel cardiovascular risk factor in kidney disease patients. 2015;13(2):229-38.
Armaly Z, Abassi ZJAiN. Deleterious effects of increased intra-abdominal pressure on kidney function. 2014;2014.
Cheatham MLJSjot, resuscitation, medicine e. Abdominal compartment syndrome: pathophysiology and definitions. 2009;17(1):10.
- There are currently no refbacks.