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Disease relevance of Nephrons

  • As a result, p53 transgenic kidneys grow to only half of their expected size and contain about half of the normal number of nephrons, with compensatory hypertrophy of the glomeruli [1].
  • The administration of acetazolamide (20 mg/kg body weight [bw]/h) decreased proximal reabsorption to 65.6% of the filtered load in superficial nephrons (32% was reabsorbed by the proximal convoluted tubule while 31.7% was reabsorbed by the loop segment), and to 38.4% in juxtamedullary nephrons [2].
  • The basement membrane of normal nephrons is similar to that in tubules of triphasic Wilms' tumor, but the ECM of blastemas is different [3].
  • This leads to impaired ability to excrete sodium by both populations of nephrons, with sodium retention in the presence of abnormal renin secretion and perpetuation of the hypertension [4].
  • In chronic renal failure, the ability to form hypertonic urine declines but is nevertheless well preserved with respect to declining GFR, thus imposing on remnant nephrons an additional permanent stimulus for hyperfiltration.(ABSTRACT TRUNCATED AT 400 WORDS)[5]

High impact information on Nephrons

  • The apparent marked capacity for compensatory growth in all nephron segments and even in portions of tubular segments in parenchymal renal disease increases the area for transport by tubular epithelia in residual nephrons, as the overall number of nephrons diminishes.. [6].
  • Aldosterone controls the final sodium reabsorption and potassium secretion in the kidney by regulating the activity of the epithelial sodium channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) [7].
  • Adenosine activity was manipulated by microperfusing nephrons with adenosine A1 receptor blocker, A1-agonist, or 5'-nucleotidase inhibitor [8].
  • Microperfusion of L-arginine (10[-3] M) into the peritubular capillaries reduced the maximum TGF response more in nephrons of LS than HS rats (deltaTGF: LS, 32+/-6 vs. HS, 13+/-4%; P < 0.05) and restored a TGF response to luminal perfusion of NG-methyl-L-arginine in LS rats [9].
  • Coperfusion of nephrons with excess L-lysine or L-homoarginine, which compete with L-arginine for system y+ transport, blocked the fall in proximal stopflow pressure produced by orthograde LH perfusion of L-arginine in LS rats [9].

Chemical compound and disease context of Nephrons

  • An increase in Na+/glucose cotransport upstream to the macula densa might contribute to the increase in single nephron GFR (SNGFR) in early diabetes mellitus by lowering the signal of the tubuloglomerular feedback, i.e., the luminal Na+, Cl-, and K+ concentration sensed by the macula densa [10].
  • The capacity of the kidney to compensate for nephron loss by hypertrophy and modification of the remaining nephrons can mask progressive renal disease and thus impair our ability to detect meaningful differences in therapeutic results [11].
  • Homozygous animals died of uremia after three to four weeks with severe cystic transformation of virtually all nephrons and collecting ducts (serum urea: 616 +/- 195 mg/dl; kidney-to-body weight ratio: > 20%) [12].
  • Whole kidney levels of albuminuria correlated closely with the frequency of luminal deposits in both LL and SL nephrons of SHRs and ADR rats and in LL nephrons of aging rats (p < .005) [13].
  • The pathogenesis of the ischemia remains to be elucidated, but reasons are advanced for favoring the view that the mechanism of cyclosporin A nephrotoxicity is primarily vasomotor, causing a reduction of renal blood flow and glomerular filtration rate without permanent organic arterial narrowing; nephrons become damaged irreversibly nevertheless [14].

Biological context of Nephrons

  • At 24 h probucol treatment (IP) improved single nephron glomerular filtration rate (SNGFR) (28.1 +/- 3.3 nl/min) in comparison to untreated ischemic (I) rats (15.2 +/- 3.0), primarily as a result of improving SNGFR in a population of low SNGFR, low flow and/or obstructed nephrons [15].
  • Na/H antiporter mRNA expression in the proximal tubule was not detectable in S1 and S2 segments from superficial and most midcortical nephrons, which exhibit exclusively luminal Na/H antiport activity [16].
  • One Wilms' tumour predisposition gene (WT1), encoding a zinc finger protein, is expressed in a limited set of tissues, including developing nephrons and gonads [17].
  • However, the cells within these structures that normally differentiate into the tubular segments of the mature nephron undergo apoptosis, resulting in the formation of kidneys with severely truncated nephrons consisting of renal corpuscles connected to collecting ducts by an abnormally short tubular segment [18].
  • However, once Gdnf stimulates branching of the ureteric bud, the Flk1-dependent angioblast signal is no longer required to maintain branching morphogenesis and induction of nephrons [19].

Anatomical context of Nephrons

  • Urea transporter UT-A2, the major urea transporter of the thin descending limb of the loop of Henle in short loop nephrons, has been implicated in urea recycling in the medulla, thereby producing concentrated urine [20].
  • At about four times the concentration required to inhibit ES-cell differentiation, LIF strongly but reversibly blocks the effects of metanephric mesenchyme induction: although mesenchyme condenses around growing duct tips, the number of mature nephrons that form over 6 days is reduced by 75% or more [21].
  • By immunohistology, podocin was detected in podocytes from the early capillary loop stage in the developing nephrons, and at the basal pole, along the GBM, in mature glomeruli [22].
  • Exogenous galectin-3 retarded conversion of renal mesenchyme to nephrons in whole metanephric explants but did not affect nephron induction by spinal cord in isolated renal mesenchymes [23].
  • UT-A2 immunoreactivity was observed mainly on the basolateral membrane of the type 1 epithelium of the descending thin limb (DTL) of short-looped nephrons [24].

Associations of Nephrons with chemical compounds

  • Structural studies demonstrated communication of dilated nephrons with cysts, concretions of debris within tubular lumens, evidence of extrinsic pressure by cysts on adjacent tubules, and apparent luminal narrowing of some proximal tubules [25].
  • No effect was detected on the fractional absorption of water, total CO2, and chloride at end-proximal and early distal sites of superficial nephrons in intact animals; dDAVP, however, inhibited the fractional absorption of total CO2 in Henle's loop while stimulating that of chloride in thyroparathyroidectomized (TPTX) somatostatin-infused rats [26].
  • Absolute reabsorption of bicarbonate was also significantly higher in superficial than in juxtamedullary nephrons after administration of acetazolamide (727 +/- 82 vs. 346 +/- 126 pmol/min; P less than 0.05) [2].
  • Single nephron GFR (SNGFR) and glomerular capillary hydraulic pressure (PGC) were measured repeatedly for 8 (PAN rats) or 31 wk (ADM rats) [27].
  • It was concluded that the elevated hydrostatic pressures in the dilated nephrons of diphenylamine-exposed kidneys were the consequence of variably severe and frequently incomplete tubular occlusion [25].

Gene context of Nephrons

  • Although ADPKD is a systemic disease, it shows a focal expression, because <1% of nephrons become cystic [28].
  • Analysis with molecular markers revealed the effective induction of tubulogenic mesenchyme; however, Pbx1(-/-) kidneys contained fewer nephrons and were characterized by expanded regions of mesenchymal condensates in the nephrogenic zone [29].
  • We showed that VEGF is a direct chemoattractant for glomerular endothelial cells towards developing nephrons [30].
  • Neither MMP-2, MMP-9 nor MT1-MMP were detected in mature nephrons [31].
  • The number of nephrons per kidney was reduced by approximately 20% in Igf1-/- mice [32].

Analytical, diagnostic and therapeutic context of Nephrons

  • Likewise, single nephron filtration rte of surface nephrons was the same in the experimental rats as in the controls [33].
  • Standard micropuncture and microdissection techniques were used to examine the function and structure of nephrons in rats whose kidneys were made cystic by dietary exposure to diphenylamine [25].
  • Thus, the observed allograft protection derived from the presence of a retained recipient native kidney supports the hypothesis that a single renal allograft contains insufficient nephrons to prevent progressive renal injury, implicating nephron supply as a major determinant of long-term allograft outcome [34].
  • This angiotensin II impairs sodium excretion (adaptive hypernatriuresis) from unaffected, adapting nephrons by promoting proximal sodium reabsorption and by inducing afferent constriction [4].
  • The development of glomerular structural abnormalities in remnant nephrons, after ablation of renal mass (subtotal nephrectomy), in rats is largely prevented by the daily injection of heparin [35].


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  2. Internephron heterogeneity for carbonic anhydrase-independent bicarbonate reabsorption in the rat. Frommer, J.P., Laski, M.E., Wesson, D.E., Kurtzman, N.A. J. Clin. Invest. (1984) [Pubmed]
  3. Extracellular matrix and epithelial differentiation of Wilms' tumor. Sariola, H., Ekblom, P., Rapola, J., Vaheri, A., Timpl, R. Am. J. Pathol. (1985) [Pubmed]
  4. Nephron heterogeneity: clue to the pathogenesis of essential hypertension and effectiveness of angiotensin-converting enzyme inhibitor treatment. Laragh, J.H. Am. J. Med. (1989) [Pubmed]
  5. Is the process of urinary urea concentration responsible for a high glomerular filtration rate? Bankir, L., Ahloulay, M., Bouby, N., Trinh-Trang-Tan, M.M., Machet, F., Lacour, B., Jungers, P. J. Am. Soc. Nephrol. (1993) [Pubmed]
  6. Functional adaptation to reduction in renal mass. Hayslett, J.P. Physiol. Rev. (1979) [Pubmed]
  7. Collecting duct-specific gene inactivation of alphaENaC in the mouse kidney does not impair sodium and potassium balance. Rubera, I., Loffing, J., Palmer, L.G., Frindt, G., Fowler-Jaeger, N., Sauter, D., Carroll, T., McMahon, A., Hummler, E., Rossier, B.C. J. Clin. Invest. (2003) [Pubmed]
  8. Adenosine formed by 5'-nucleotidase mediates tubuloglomerular feedback. Thomson, S., Bao, D., Deng, A., Vallon, V. J. Clin. Invest. (2000) [Pubmed]
  9. Macula densa arginine delivery and uptake in the rat regulates glomerular capillary pressure. Effects of salt intake. Welch, W.J., Wilcox, C.S. J. Clin. Invest. (1997) [Pubmed]
  10. Glomerular hyperfiltration in experimental diabetes mellitus: potential role of tubular reabsorption. Vallon, V., Richter, K., Blantz, R.C., Thomson, S., Osswald, H. J. Am. Soc. Nephrol. (1999) [Pubmed]
  11. Overview of pediatric nephropathology. Silva, F.G. Kidney Int. (1988) [Pubmed]
  12. Characterization of the Han:SPRD rat model for hereditary polycystic kidney disease. Schäfer, K., Gretz, N., Bader, M., Oberbäumer, I., Eckardt, K.U., Kriz, W., Bachmann, S. Kidney Int. (1994) [Pubmed]
  13. Immunomorphometric studies of proteinuria in individual deep and superficial nephrons of rats. Hoyer, J.R., Fogo, A.B., Terrell, C.H., Delaney, M.M. Lab. Invest. (2000) [Pubmed]
  14. Kidney pathology in liver allograft recipients after long-term treatment with cyclosporin A. Dische, F.E., Neuberger, J., Keating, J., Parsons, V., Calne, R.Y., Williams, R. Lab. Invest. (1988) [Pubmed]
  15. Ischemic acute renal failure and antioxidant therapy in the rat. The relation between glomerular and tubular dysfunction. Bird, J.E., Milhoan, K., Wilson, C.B., Young, S.G., Mundy, C.A., Parthasarathy, S., Blantz, R.C. J. Clin. Invest. (1988) [Pubmed]
  16. Na/H antiporter mRNA expression in single nephron segments of rat kidney cortex. Krapf, R., Solioz, M. J. Clin. Invest. (1991) [Pubmed]
  17. Wilms' tumour: reconciling genetics and biology. Van Heyningen, V., Hastie, N.D. Trends Genet. (1992) [Pubmed]
  18. FGF8 is required for cell survival at distinct stages of nephrogenesis and for regulation of gene expression in nascent nephrons. Grieshammer, U., Cebrián, C., Ilagan, R., Meyers, E., Herzlinger, D., Martin, G.R. Development (2005) [Pubmed]
  19. Angioblast-mesenchyme induction of early kidney development is mediated by Wt1 and Vegfa. Gao, X., Chen, X., Taglienti, M., Rumballe, B., Little, M.H., Kreidberg, J.A. Development (2005) [Pubmed]
  20. Impaired urea accumulation in the inner medulla of mice lacking the urea transporter UT-A2. Uchida, S., Sohara, E., Rai, T., Ikawa, M., Okabe, M., Sasaki, S. Mol. Cell. Biol. (2005) [Pubmed]
  21. LIF, the ES-cell inhibition factor, reversibly blocks nephrogenesis in cultured mouse kidney rudiments. Bard, J.B., Ross, A.S. Development (1991) [Pubmed]
  22. Podocin localizes in the kidney to the slit diaphragm area. Roselli, S., Gribouval, O., Boute, N., Sich, M., Benessy, F., Attié, T., Gubler, M.C., Antignac, C. Am. J. Pathol. (2002) [Pubmed]
  23. Galectin-3 modulates ureteric bud branching in organ culture of the developing mouse kidney. Bullock, S.L., Johnson, T.M., Bao, Q., Hughes, R.C., Winyard, P.J., Woolf, A.S. J. Am. Soc. Nephrol. (2001) [Pubmed]
  24. Expression of urea transporters in potassium-depleted mouse kidney. Jung, J.Y., Madsen, K.M., Han, K.H., Yang, C.W., Knepper, M.A., Sands, J.M., Kim, J. Am. J. Physiol. Renal Physiol. (2003) [Pubmed]
  25. Function and structure in the diphenylamine-exposed kidney. Gardner, K.D., Solomon, S., Fitzgerrel, W.W., Evan, A.P. J. Clin. Invest. (1976) [Pubmed]
  26. Effects of antidiuretic hormone on urinary acidification and on tubular handling of bicarbonate in the rat. Bichara, M., Mercier, O., Houillier, P., Paillard, M., Leviel, F. J. Clin. Invest. (1987) [Pubmed]
  27. Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis. Fogo, A., Yoshida, Y., Glick, A.D., Homma, T., Ichikawa, I. J. Clin. Invest. (1988) [Pubmed]
  28. A loss-of-function model for cystogenesis in human autosomal dominant polycystic kidney disease type 2. Torra, R., Badenas, C., San Millán, J.L., Pérez-Oller, L., Estivill, X., Darnell, A. Am. J. Hum. Genet. (1999) [Pubmed]
  29. Pbx1 regulates nephrogenesis and ureteric branching in the developing kidney. Schnabel, C.A., Godin, R.E., Cleary, M.L. Dev. Biol. (2003) [Pubmed]
  30. Ontogeny of semaphorins 3A and 3F and their receptors neuropilins 1 and 2 in the kidney. Villegas, G., Tufro, A. Mech. Dev. (2002) [Pubmed]
  31. Regulated expression of matrix metalloproteinases and TIMP in nephrogenesis. Tanney, D.C., Feng, L., Pollock, A.S., Lovett, D.H. Dev. Dyn. (1998) [Pubmed]
  32. Insulin-like growth factor I regulates renal development in rodents. Rogers, S.A., Powell-Braxton, L., Hammerman, M.R. Dev. Genet. (1999) [Pubmed]
  33. A micropuncture study of renal salt and water retention in chronic bile duct obstruction. Bank, N., Aynedjian, H.S. J. Clin. Invest. (1975) [Pubmed]
  34. Nephron supply is a major determinant of long-term renal allograft outcome in rats. Mackenzie, H.S., Tullius, S.G., Heemann, U.W., Azuma, H., Rennke, H.G., Brenner, B.M., Tilney, N.L. J. Clin. Invest. (1994) [Pubmed]
  35. Effect of heparin on the glomerular structure and function of remnant nephrons. Ichikawa, I., Yoshida, Y., Fogo, A., Purkerson, M.L., Klahr, S. Kidney Int. (1988) [Pubmed]
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