Kidney Function

Nutritional considerations form an integral part in the care of a patient with kidney disease because of the kidney’s central role in dietary metabolism. Not only can dietary manipulations ameliorate the signs and symptoms of kidney disease, but they also form an important adjunct of therapy regardless of the degree of decrease in kidney function. Whether the patient has chronic kidney disease (CKD) not yet requiring dialysis therapy, is undergoing renal replacement therapy, or has received a kidney transplant, timely and appropriate nutritional intervention can optimize patient care and outcomes. Last, nutritional markers, such as serum albumin, are highly predictive of morbidity and mortality and further emphasize the importance of nutritional concerns in the management of patients with kidney disease.

Imaging studies show entrapment of the left renal vein in the fork between the aorta and proximal superior mesenteric artery in most cases of isolated postural proteinuria. Therefore, it has been postulated that partial obstruction to the flow in the left renal vein in the upright position is a cause of this form of proteinuria. In a girl with isolated postural proteinuria, kidney ultrasonic imaging and Doppler flow scanning showed left renal vein entrapment. Seven years later, a new evaluation showed resolution of both postural proteinuria and left renal vein entrapment. The longitudinal observation provides substantial additional support for entrapment of the left renal vein by the aorta and superior mesenteric artery as a cause of isolated postural proteinuria.

Background: Nephrogenic systemic fibrosis (NSF) is an uncommon fibrotic disorder occurring after administration of linear gadolinium contrast agents in patients with severely decreased kidney function. The underlying pathogenetic mechanism of fibrosis remains to be elucidated. Transforming growth factor β (TGF-β), a key player in the pathogenesis of fibrotic disorders, has been found to be overexpressed in NSF skin lesions. The aim of this study is to analyze the TGF-β–SMAD–connective tissue growth factor (CTGF) axis in NSF skin lesions compared with skin specimens from patients with systemic sclerosis, hemodialysis patients without NSF, and healthy controls. Additionally, expression of tissue inhibitor of metalloproteinase 1 (TIMP-1) and antifibrotic tumor necrosis factor α (TNF-α) were examined.Study Design: Observational study.Setting & Participants: Full-thickness skin biopsy specimens from fibrotic lesions or healthy skin were obtained from 10 patients with NSF, 16 patients with systemic sclerosis, 8 non-NSF hemodialysis patients, and 17 healthy participants.Predictor: Patient diagnosis of NSF, systemic sclerosis, non-NSF hemodialysis patients, and healthy participants, as defined using skin biopsy.Outcome & Measurements: Dermal messenger RNA and protein expression of profibrotic TGF-β, SMAD2, SMAD3, SMAD4, SMAD7, CTGF, TIMP-1, antifibrotic SMAD7, and TNF-α were analyzed using real-time reverse transcription–polymerase chain reaction and immunohistologic examination on formalin-embedded tissue.Results: Dermal expression of nearly all parameters differed in hemodialysis patients compared with healthy controls. In comparison to hemodialysis patients and healthy participants, we found increased messenger RNA levels for TGF-β, the profibrotic receptor-activated SMAD2 and SMAD3, CTGF, and TIMP-1 in NSF and systemic sclerosis lesions. Few differences between NSF and non-NSF hemodialysis patients were observed for common SMAD4, inhibitory SMAD7, and TNF-α.Limitations: Small patient cohort.Conclusion: Our results suggest a profibrotic imbalance in the TGF-β–SMAD-CTGF axis in NSF skin lesions. Significantly increased dermal expression of TGF-β and TIMP-1 in non-NSF hemodialysis patients in comparison to healthy participants emphasizes the need for a hemodialysis control group for future investigations and suggests a pre-existing profibrotic situation in the skin of hemodialysis patients.