Glomerular hyperfiltration is a situation where the filtration elements in the kidneys called glomeruli produce excessive amounts of pro-urine. It can be part of a number of medical conditions particularly diabetic nephropathy (kidney damage associated with diabetes).[1]
| Glomerular hyperfiltration | |
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| Diagram showing a schematic nephron and its blood supply. |
There is no universally accepted definition of glomerular hyperfiltration, and little research has been done on the pathophysiological mechanisms, which are likely to change depending on the underlying ailment.[2]
Glomerular hyperfiltration can result from efferent arteriolar vasoconstriction due to activation of the renin-angiotensin-aldosterone system, which causes glomerular hypertension, or afferent arteriolar vasodilation, as observed in diabetic patients or following a high-protein meal.[2]
Causes
editIn healthy individuals, high protein loading causes glomerular hyperfiltration, or an absolute increase in glomerular filtration rate (GFR).[3]
Risk factors
editMost young Type 1 diabetic patients experience glomerular hyperfiltration, a typical functional deviation in insulin-dependent diabetes mellitus.[4] A meta-analysis of research done on Type 1 diabetic subjects found that people with glomerular hyperfiltration have a higher chance of developing albuminuria and seeing their diabetic nephropathy worsen.[5] Poor glycaemic control has been blamed for this finding because hyperfiltration and HbA1c were found to be correlated.[6]
According to certain research, glomerular hyperfiltration happens in cases of hypertension as well.[7] Humans with early-stage hypertension have demonstrated glomerular hyperfiltration during sympathetic nervous system activation.[8]
Mechanism
editActivation of the renin-angiotensin-aldosterone system may be the mechanism underlying renal injury linked to glomerular hyperfiltration. This can result in endothelial dysfunction, increased arterial stiffness, and maladaptive renal and systemic hemodynamic responses.[9][10]
Diagnosis
editThe lack of an established definition for this clinical entity is one of the primary issues with the diagnosis of hyperfiltration.[11] The primary cause of the lack of clarity surrounding the GFR levels that indicate hyperfiltration is their strong reliance on age.[12] Glomerular hyperfiltration has traditionally been characterized as an elevated whole-kidney GFR, or a GFR greater than two standard deviations above the mean GFR of healthy individuals.[2]
Treatment
editIn diabetic mice, proinsulin C-peptide, a putative renoprotective agent, narrows glomerular afferent arterioles. Therefore, proinsulin C-peptide administration should theoretically prevent glomerular hyperfiltration.[13]
An insulin-sensitizing medication called rosiglitazone is known to treat endothelial dysfunction. It has been demonstrated that this medication reduces renal end-organ damage in patients with type 2 diabetes and microalbuminuria, improves nitric oxide bioavailability, and ameliorates glomerular hyperfiltration in patients with early type 2 diabetes.[14]
In experimental diabetes, renal nerves may play a significant role in mediating glomerular hyperfiltration. In this sense, in diabetic rats, chronic renal denervation also inhibits glomerular hyperfiltration.[15]
See also
editReferences
edit- ^ Cachat, F; Combescure, C; Cauderay, M; Girardin, E; Chehade, H (7 January 2015). "A Systematic Review of Glomerular Hyperfiltration Assessment and Definition in the Medical Literature". Clinical Journal of the American Society of Nephrology. 10 (3): 382–9. doi:10.2215/CJN.03080314. PMC 4348676. PMID 25568216.
- ^ a b c Helal, Imed; Fick-Brosnahan, Godela M.; Reed-Gitomer, Berenice; Schrier, Robert W. (February 21, 2012). "Glomerular hyperfiltration: definitions, mechanisms and clinical implications". Nature Reviews Nephrology. 8 (5). Springer Science and Business Media LLC: 293–300. doi:10.1038/nrneph.2012.19. ISSN 1759-5061. PMID 22349487. S2CID 5678191.
- ^ BERGSTRÖM, JONAS; AHLBERG, MARIANNE; ALVESTRAND, ANDERS (January 12, 1985). "Influence of Protein Intake on Renal Hemodynamics and Plasma Hormone Concentrations in Normal Subjects". Acta Medica Scandinavica. 217 (2). Wiley: 189–196. doi:10.1111/j.0954-6820.1985.tb01655.x. ISSN 0001-6101. PMID 3887848.
- ^ Amin, Rakesh; Turner, Charles; van Aken, Sara; Konopelska Bahu, Teresa; Watts, Angela; Lindsell, David R.M.; Neil Dalton, R.; Dunger, David B. (2005). "The relationship between microalbuminuria and glomerular filtration rate in young type 1 diabetic subjects: The Oxford Regional Prospective Study". Kidney International. 68 (4). Elsevier BV: 1740–1749. doi:10.1111/j.1523-1755.2005.00590.x. ISSN 0085-2538. PMID 16164650.
- ^ Magee, G. M.; Bilous, R. W.; Cardwell, C. R.; Hunter, S. J.; Kee, F.; Fogarty, D. G. (February 7, 2009). "Is hyperfiltration associated with the future risk of developing diabetic nephropathy? A meta-analysis". Diabetologia. 52 (4). Springer Science and Business Media LLC: 691–697. doi:10.1007/s00125-009-1268-0. ISSN 0012-186X. PMID 19198800.
- ^ DAHLQUIST, G.; APERIA, A.; BROBERGER, O.; PERSSON, B.; WILTON, P. (1983). "Renal Function in Relation to Metabolic Control in Children with Diabetes of Different Duration". Acta Paediatrica. 72 (6). Wiley: 903–909. doi:10.1111/j.1651-2227.1983.tb09838.x. ISSN 0803-5253. PMID 6369870. S2CID 37840032.
- ^ QUASCHNING, THOMAS; D'USCIO, LIVIUS V.; SHAW, SIDNEY; GRÖNE, HERMANN-JOSEF; RUSCHITZKA, FRANK; LÜSCHER, THOMAS F. (2001). "Vasopeptidase Inhibition Restores Renovascular Endothelial Dysfunction in Salt-Induced Hypertension". Journal of the American Society of Nephrology. 12 (11). Ovid Technologies (Wolters Kluwer Health): 2280–2287. doi:10.1681/asn.v12112280. ISSN 1046-6673. PMID 11675404.
- ^ Schmieder, R E; Veelken, R; Schobel, H; Dominiak, P; Mann, J F; Luft, F C (1997). "Glomerular hyperfiltration during sympathetic nervous system activation in early essential hypertension". Journal of the American Society of Nephrology. 8 (6). Ovid Technologies (Wolters Kluwer Health): 893–900. doi:10.1681/asn.v86893. ISSN 1046-6673. PMID 9189855.
- ^ Cherney, David Z.I.; Lai, Vesta; Scholey, James W.; Miller, Judith A.; Zinman, Bernard; Reich, Heather N. (November 4, 2009). "Effect of Direct Renin Inhibition on Renal Hemodynamic Function, Arterial Stiffness, and Endothelial Function in Humans With Uncomplicated Type 1 Diabetes". Diabetes Care. 33 (2). American Diabetes Association: 361–365. doi:10.2337/dc09-1303. ISSN 0149-5992. PMC 2809283. PMID 19889802.
- ^ van der Meer, Irene M; Cravedi, Paolo; Remuzzi, Giuseppe (May 4, 2010). "The role of renin angiotensin system inhibition in kidney repair". Fibrogenesis & Tissue Repair. 3 (1). Springer Science and Business Media LLC: 7. doi:10.1186/1755-1536-3-7. ISSN 1755-1536. PMC 2888753. PMID 20441574.
- ^ Palatini, P. (March 19, 2012). "Glomerular hyperfiltration: a marker of early renal damage in pre-diabetes and pre-hypertension". Nephrology Dialysis Transplantation. 27 (5). Oxford University Press (OUP): 1708–1714. doi:10.1093/ndt/gfs037. ISSN 0931-0509. PMID 22431709.
- ^ Premaratne, E.; MacIsaac, R. J.; Tsalamandris, C.; Panagiotopoulos, S.; Smith, T.; Jerums, G. (November 1, 2005). "Renal hyperfiltration in type 2 diabetes: effect of age-related decline in glomerular filtration rate". Diabetologia. 48 (12). Springer Science and Business Media LLC: 2486–2493. doi:10.1007/s00125-005-0002-9. ISSN 0012-186X. PMID 16261309.
- ^ Nordquist, Lina; Lai, En Yin; Sjöquist, Mats; Patzak, Andreas; Persson, A. Erik G. (2008). "Proinsulin C-peptide constricts glomerular afferent arterioles in diabetic mice. A potential renoprotective mechanism". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 294 (3). American Physiological Society: R836–R841. doi:10.1152/ajpregu.00811.2007. ISSN 0363-6119. PMID 18077505.
- ^ Pistrosch, Frank; Herbrig, Kay; Kindel, Beate; Passauer, Jens; Fischer, Sabine; Gross, Peter (July 1, 2005). "Rosiglitazone Improves Glomerular Hyperfiltration, Renal Endothelial Dysfunction, and Microalbuminuria of Incipient Diabetic Nephropathy in Patients". Diabetes. 54 (7). American Diabetes Association: 2206–2211. doi:10.2337/diabetes.54.7.2206. ISSN 0012-1797. PMID 15983223.
- ^ Luippold, G. (February 1, 2004). "Chronic renal denervation prevents glomerular hyperfiltration in diabetic rats". Nephrology Dialysis Transplantation. 19 (2). Oxford University Press (OUP): 342–347. doi:10.1093/ndt/gfg584. ISSN 1460-2385. PMID 14736957.
Further reading
edit- Chagnac, Avry; Zingerman, Boris; Rozen-Zvi, Benaya; Herman-Edelstein, Michal (2019). "Consequences of Glomerular Hyperfiltration: The Role of Physical Forces in the Pathogenesis of Chronic Kidney Disease in Diabetes and Obesity". Nephron. 143 (1). S. Karger AG: 38–42. doi:10.1159/000499486. ISSN 1660-8151. PMID 30947190.
- Cortinovis, Monica; Perico, Norberto; Ruggenenti, Piero; Remuzzi, Andrea; Remuzzi, Giuseppe (April 1, 2022). "Glomerular hyperfiltration". Nature Reviews Nephrology. 18 (7). Springer Science and Business Media LLC: 435–451. doi:10.1038/s41581-022-00559-y. ISSN 1759-5061. PMID 35365815. S2CID 247860806.