Neuroendocrine adaptations in renal disease

Feneberg, Reinhard; Schaefer, Franz; Veldhuis, Johannes D.

doi:10.1007/s00467-003-1160-y

Cited by 19 publications

(11 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There may also be postreceptor defects as for insulin [68]. Adding to this complexity, alterations in the circadian rhythm or the time-dependent secretion of several hormones have been described [69,70]. In summary, altered regulation of hormones modulating insulin action may contribute to the IR found in CRF.…”

Section: Does Diabetic Nephropathy (Dn) Cause Insulin Resistance (Ir)?mentioning

confidence: 92%

Insulin resistance in diabetic nephropathy — cause or consequence?

Svensson

Eriksson

2006

Diabetes Metabolism Res

View full text Add to dashboard Cite

Insulin resistance (IR) is associated with multiple risk factors for cardiovascular disease. Many studies have shown that IR is present in chronic renal failure (CRF), and recent evidence suggests that IR can also occur in the early stages of renal disease. Patients with diabetic nephropathy (DN) have an increase in cardiovascular mortality, and since IR may be a contributing factor, this emphasizes the importance of a detailed understanding of the mechanisms linking IR and renal dysfunction at different stages of DN. IR can be detected early on in DN, e.g. at the stage of microalbuminuria (MA) and this could indicate a common genetic trait for IR and DN. As DN progresses further, IR is aggravated and it may, in addition to other factors, possibly accelerate the decline in renal function toward end-stage renal disease (ESRD). Several potentially modifiable mechanisms including circulating hormones, neuroendocrine pathways and chronic inflammation, are said to contribute to the worsening of IR. In ESRD, uremic toxins are of major importance. In this review article, we address the association between different stages of DN and IR and attempt to summarize major findings on potential mechanisms linking DN and IR. We conclude that IR is a consequence, and potentially also a cause of DN. In addition, there are probably genetic and environmental background factors that predispose to both IR and DN.

show abstract

Section: Does Diabetic Nephropathy (Dn) Cause Insulin Resistance (Ir)?mentioning

confidence: 92%

Insulin resistance in diabetic nephropathy — cause or consequence?

Svensson

Eriksson

2006

Diabetes Metabolism Res

View full text Add to dashboard Cite

show abstract

“…In CRF, GH production may be reduced, normal or, under certain conditions, even increased [12]. In late prepubertal and pubertal children with CRF, GH secretion is normal or low [13].…”

Section: Gh and Igf-1 Levels In Renal Failurementioning

confidence: 96%

Growth hormone resistance in uremia, a role for impaired JAK/STAT signaling

et al. 2005

Self Cite

View full text Add to dashboard Cite

Resistance to growth hormone (GH) is a significant complication of advanced chronic renal failure. Thus while the circulating GH levels are normal or even elevated in uremia, resistance to the hormone leads to stunting of body growth in children and contributes to muscle wasting in adults. Insensitivity to GH is the consequence of multiple defects in the GH/insulin-like growth factor-1 (IGF-1) system. Expression of the GH receptor may be reduced, although this is not a consistent finding, GH activation of the Janus kinase 2-signal transducer (JAK2) and activator of transcription (STAT) signal transduction pathway is depressed and this leads to reduced IGF-1 expression, and finally there is resistance to IGF-1, a major mediator of GH action. We review these various defects with an emphasis on the GH-activated JAK2-STAT5 pathway, since this pathway is essential for normal body growth and there has been recent progress in our understanding of the perturbations that occur in uremia.

show abstract

“…Circulating levels of GH are a balance between the production rate and metabolic clearance. GH synthesis may be reduced, normal, or even increased in CKD [35]. GH secretion is normal or low in late pre-pubertal and pubertal children with CRF [36]; whereas GH secretion rates are increased with increased GH burst frequency in pre-pubertal children and in adults with end-stage renal disease (ESRD) [36][37][38].…”

Section: Gh and Igf-i Circulating Levels In Ckdmentioning

confidence: 99%

The growth hormone–insulin-like growth factor-I axis in chronic kidney disease

Mak

Cheung

Roberts

2008

Growth Hormone & IGF Research

View full text Add to dashboard Cite

Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are important physiologic regulators of growth, body composition, and kidney function. Perturbations in the GH-IGF-I axis are responsible for many important complications seen in chronic kidney disease (CKD), such as growth retardation and cachectic wasting, as well as disease progression. Recent evidence suggests that CKD is characterized by abnormalities in GH and IGF-I signal transduction and the interaction of these pathways with those that involve other molecules such as ghrelin, myostatin, and the suppressor of cytokine signaling (SOCS) family. Further understanding of GH/IGF pathophysiology in CKD may lead to the development of therapeutic strategies for these devastating complications, which are associated with high rates of mortality and morbidity.

show abstract

Neuroendocrine adaptations in renal disease

Cited by 19 publications

References 35 publications

Insulin resistance in diabetic nephropathy — cause or consequence?

Insulin resistance in diabetic nephropathy — cause or consequence?

Growth hormone resistance in uremia, a role for impaired JAK/STAT signaling

The growth hormone–insulin-like growth factor-I axis in chronic kidney disease

Contact Info

Product

Resources

About