Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Xenotransplantation can provide a solution to the current shortage of human organs for patients with terminal renal failure. The increasing availability of genetically engineered pigs, effective immunosuppressive therapy, and antiinflammatory therapy help to protect pig tissues from the primate immune response and can correct molecular incompatibilities. Life-supporting pig kidney xenografts have survived in NHP for more than 6 mo in the absence of markers of consumptive coagulopathy. However, few reports have focused on the physiologic aspects of life-supporting pig kidney xenografts. We have reviewed the literature regarding pig kidney xenotransplantation in NHP. The available data indicate (1) normal serum creatinine, (2) normal serum electrolytes, except for a trend toward increased calcium levels and a transient rise in phosphate followed by a fall to slightly subnormal values, (3) minimal or modest proteinuria without hypoalbuminemia (suggesting that previous reports of proteinuria likely were due to a low-grade immune response rather than physiologic incompatibilities), (4) possible discrepancies between pig erythropoietin and the primate erythropoietin receptor, and (5) significant early increase in kidney graft size, which might result from persistent effects of pig growth hormone. Further study is required regarding identification and investigation of physiologic incompatibilities. However, current evidence suggests that, in the absence of an immune response, a transplanted pig kidney likely would satisfactorily support a human patient.
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PMID:Physiologic Aspects of Pig Kidney Transplantation in Nonhuman Primates. 3020 86

In Type 1 diabetes, poor glycemic control is the key predictor for the development of microalbuminuria, an established early marker of overt nephropathy. However, the role of other pathways in the development of diabetic nephropathy may also be important. The growth hormone (GH) hypothesis suggests that the GH-insulin-like growth factor (IGF)-1 axis may play an important role in this disease process. In Type 1 diabetes, the characteristic pattern of GH hypersecretion and low circulating IGF-1 levels results from hepatic GH resistance owing to the lack of portal insulin. Clinical data indicate that high GH and low IGF-1 levels reduce insulin sensitivity and worsen glycemic control. Furthermore, despite hepatic GH resistance, GH receptors at the kidney remain intact. Experimental data show that excess GH stimulates renal GH receptors and, through paracrine IGF-1 production, results in pathophysiological changes consistent with diabetic nephropathy, namely nephromegaly, glomerular hyperfiltration and eventual proteinuria. These abnormalities are reversed by intervention to block or normalize the local effects of GH and IGF-1. Although such data in humans are limited, preliminary trials show that interventions to increase IGF-1 levels and reduce GH hypersecretion improve glycemic control and insulin sensitivity in the short term. However, their effects on early nephropathy and end points, such as the prevalence of end stage renal disease, have yet to be determined.
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PMID:Growth hormone hypothesis and development of diabetic nephropathy in Type 1 diabetes. 3075 96

Acromegaly is characterized by autonomous excessive growth hormone (GH) secretion, generally due to GH-producing pituitary adenoma, and is associated with various systemic comorbidities including diabetes mellitus. Polycystic kidney disease (PKD) is characterized by the growth of numerous cysts in the kidneys that deteriorate renal function. While possible renal effects of excessive GH exposure have been a current issue in experimental medicine, only five cases of coexisting acromegaly and PKD have been reported previously, and little is known regarding the influence of acromegaly on renal disease. We treated a 50-year-old male with diabetes mellitus who showed a sudden and rapid decline of renal function along with increasing proteinuria, which led to diagnoses of PKD and acromegaly. His urinary protein levels were increased together with excessive GH secretion and worsening glycemic control. An increase of total kidney volume was also noted. Transsphenoidal surgery for the pituitary adenoma was successfully performed. Marked improvement of hyperglycemia and proteinuria were observed after the surgery, but renal function was unchanged. The patient's clinical course suggested common aspects of excessive GH secretion as an accelerating factor of the progression of diabetic nephropathy and PKD via direct and indirect pathways. Although coexisting acromegaly and PKD is clinically rare, vigilance for early diagnosis of acromegaly is appropriate in patients with diabetes and/or PKD, especially in those showing unexpected exacerbation of renal dysfunction.
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PMID:Acromegaly accompanied by diabetes mellitus and polycystic kidney disease. 3281 22

Growth failure is a hallmark in children with chronic kidney disease (CKD). Therefore, early diagnosis and adequate management of growth failure is of utmost importance in these patients. The risk of severe growth retardation is the higher the younger the child is, which places an additional burden on patients and their families and hampers the psychosocial integration of these children. Careful monitoring of growth, and effective interventions are mandatory to prevent and treat growth failure in children with CKD at all ages and all stages of kidney failure. Early intervention is critical, as all therapeutic interventions are much more effective if they are started prior to the initiation of dialysis. Prevention and treatment of growth failure focuses on: (i) preservation of renal function, e.g., normalization of blood pressure and proteinuria by use of inhibitors of the renin-angiotensin aldosterone system, (ii) adequate energy intake, including tube feeding or gastrostomy in case of persisting malnutrition, (iii) substitution of water and electrolytes, especially in children with renal malformation, (iv) correction of metabolic acidosis, (v) control of parathyroid hormone levels within the CKD-dependent target range, (vi) use of recombinant human growth hormone in cases of persistent growth failure, and, (vii) early/preemptive kidney transplantation using steroid-minimizing immunosuppressive protocols in children with end-stage CKD. This review discusses these measures based on recent guidelines.
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PMID:Strategies for Optimizing Growth in Children With Chronic Kidney Disease. 3285 May 27


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