Metabolic adaptations of the nephron in renal disease

Klahr, Saulo; Schwab, Sidney I.; Stokes, Thomas J.

doi:10.1038/ki.1986.10

Cited by 28 publications

(13 citation statements)

References 74 publications

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“…However, it is difficult to cor relate CanAg to chronic pancreatitis which may occur in uremia since that inflammatory process is not associated with a sustained increase in CanAg levels [27][28][29]. A speculation still unexplored might take into consider ation the possibility that the uremic state per se may induce the formation of a new carbohydrate structure due to activation of normally unexpressed glycosyl-transferases; such a speculation is in agreement with the concept of uremia as a molecular disease [37] and with the data in rats with various experimental models of renal diseases (urinary tract obstruction, nephrotoxic or ischemicinduced acute renal failure, chronic models of renal fail ure), where enzymatic stimulation/depression has been shown [38], These studies showed a decrease/increase of (a) energy and substrate metabolism; (b) activity of en zymes; (c) hormonal responses/activities, and (d) lipid metabolism. It is of particular interest that evidence was presented for increased anaerobic glycolysis and synthe sis of triglycerides, glucose-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, LDH 4,5 isoenzymes; renin and erythropoietin secretion and synthesis of pros taglandin.…”

Section: T T T T T T T T T T T 2 0 -• • T T T T T T • •supporting

confidence: 64%

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and α-Fetoprotein

DeSanto¹,

Veneroso²,

Capodicasa³

et al. 1986

Am J Nephrol

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The incidence of the tumor markers was studied in 140 patients aged between 18 and 84 years who had been on dialysis for 4–188 months. Neuron-specific enolase increased in 81 cases, CA-50 carbohydrate antigen in 44, while α-fetoprotein was within the normal range. Carcinoembryonic antigen (CEA) with 2 monoclonal assays was increased in 7 cases. When polyclonal assays were used, CEA was found to be elevated in 12 cases with one set and in 72 cases with another kit set. The data point (1) to the potential usefulness of these markers for the detection of malignancy and possibly neuropathy in uremia; (2) to the importance of renal tubules in the metabolism of proteins, glycoprotein and peptides, and (3) to the activation/inhibition in various enzyme systems in the uremic state.

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Section: T T T T T T T T T T T 2 0 -• • T T T T T T • •supporting

confidence: 64%

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and α-Fetoprotein

DeSanto¹,

Veneroso²,

Capodicasa³

et al. 1986

Am J Nephrol

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“…While there is no real evidence to support the fact that degradation of glycoproteins is reduced in chronic renal failure [ 13], it cannot be excluded that the reticuloendothial system is compromised in uremia; this would be comparable to the elevation of CEA in chronic liver disease. However, TPA levels are also elevated in benign proliferative pro cesses, such as pregnancy [14] or postoperative wound healing [10].…”

Section: Discussionmentioning

confidence: 93%

Elevated Tumor Markers in Hemodialysis Patients

Walz¹,

Kunzendorf²,

Keller

et al. 1988

Am J Nephrol

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The incidence of elevated tumor markers without clinical signs of malignant disease was examined in 93 patients between the age of 29 and 79 years and on chronic dialysis for 3–240 months. Tissue polypeptide antigen was found to be elevated in 92.5%, carcinoembryonic antigen in 29.8, and α-fetoprotein in 6.5%. High levels of tissue polypeptide antigen were accompanied by high levels of β₂-microglobulin (p < 0.005). This indicates that tumor markers, and tissue polypeptide antigen in particular, may be unreliable for monitoring malignant disease in patients on hemodialysis.

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“…Since functionality is compromised in the obstructed kidney of the UUO model, the C/L undergoes various haemodynamic, structural and functional adaptations to persevere clearance and maintain homeostasis 40, 45, 46 . Accordingly, the circulating concentrations of phosphate, calcium, as well as calcitriol, PTH and intact FGF23 were unchanged by UUO.…”

Section: Discussionmentioning

confidence: 99%

FGF23 is synthesised locally by renal tubules and activates injury-primed fibroblasts

Smith

Tan

Holt

et al. 2017

Sci Rep

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In kidney disease, higher circulating levels of the mineral-regulating hormone fibroblast growth factor (FGF)-23 are predictive of disease progression but direct pathogenic effects on the kidney are unknown. We sought evidence of local renal synthesis in response to unilateral ureteric obstruction in the mouse, and pro-fibrotic actions of FGF23 on the fibroblast in vitro. Acute tubulointerstitial injury due to unilateral ureteric obstruction stimulated renal FGF23 synthesis by tubules, and downregulated inactivating proprotein convertases, without effects on systemic mineral metabolism. In vitro, FGF23 had divergent effects on fibroblast activation in cells derived from normal and obstructed kidneys. While FGF23 failed to stimulate fibrogenesis in normal fibroblasts, in those primed by injury, FGF23 induced pro-fibrotic signalling cascades via activation of TGF-β pathways. Effects were independent of α-klotho. Tubule-derived FGF23 may amplify myofibroblast activation in acute renal injury, and might provide a novel therapeutic target in renal fibrosis.

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Metabolic adaptations of the nephron in renal disease

Cited by 28 publications

References 74 publications

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and α-Fetoprotein

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and α-Fetoprotein

Elevated Tumor Markers in Hemodialysis Patients

FGF23 is synthesised locally by renal tubules and activates injury-primed fibroblasts

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Metabolic adaptations of the nephron in renal disease

Cited by 28 publications

References 74 publications

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and &alpha;-Fetoprotein

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and &alpha;-Fetoprotein

Elevated Tumor Markers in Hemodialysis Patients

FGF23 is synthesised locally by renal tubules and activates injury-primed fibroblasts

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Product

Resources

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Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and α-Fetoprotein

Tumor Markers in Uremia: Carcinoembryonic Antigen, Neuron-Specific Enolase, Carbohydrate Antigen CA-50 and α-Fetoprotein