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Therapeutic apheresis
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Following transplantation, the initial underlying disease, such as focal segmental glomerulosclerosis (FSGS), can recur in the allograft. Recurrent FSGS occurs in 30% of allografts, and is thought to be mediated by a circulating 50 kDa factor that causes increased glomerular permeability.70 Although controlled trials have not been performed, there are multiple case reports and case series describing the use of plasma exchange for recurrent FSGS.71 In the majority of cases, improvement of disease (elimination or decrease in proteinuria and stabilization of renal function) was achieved. In most cases, treatment consisted of 6–14 exchanges over 1–2 weeks, initiated shortly after the reappearance of proteinuria. Alternatively, immunoadsorption with Staphylococcus protein A or anti-IgG columns have also been reported to be efficacious.72–73
PMM2-CDG (Congenital disorders of glycosylation, type Ia)
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Clinical laboratory evaluation may reveal proteinuria. There is often an intermittent thrombocytosis, with counts up to 800,000 per mm3. There may be hypoprothrombinemia and diminished factors IX and XI. Elevated transaminases typically normalize after the first two years of life but become elevated during illness. Serum albumin is usually low, and some have a hypo-β-lipoproteinemia. The stroke-like episodes and thrombotic disease have been associated with decreased levels of protein C and antithrombin III and other major inhibitors of coagulation [18]. Thyroxine-binding globulin (TBG) is reduced in 75 percent of patients. CSF protein may be elevated. In general, patients with CDG are clinically euthyroid but may present with the biochemical picture of partial TGB deficiency (low total T4, normal free T4, normal thyroid-stimulating hormone [TSH]). These patients require no treatment unless they present with elevated TSH and low free T4.
Personalized Nutrition in Chronic Kidney Disease
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Proteinuria is a sign of kidney disease. While low-grade proteinuria may be a sign of interstitial damage, proteinuria over 1 g per day is highly likely to be of glomerular origin. Proteinuria is both a sign of kidney disease and a progression factor, and its presence and degree is a therapeutic target in CKD (Kincaid-Smith and Fairley 2005; Cirillo 2010; Gorriz and Martinez-Castelao 2012; Cyriac, Holden et al. 2017).
Standardized aqueous stem bark extract of Gmelina arborea roxb. possesses nephroprotection against adriamycin-induced nephrotoxicity in Wistar rats
Published in Drug and Chemical Toxicology, 2022
Sachinthi S. Amarasiri, Anoja P. Attanayake, Liyanagae D. A. M. Arawwawala, Kamani A. P. W. Jayatilaka, Lakmini K. B. Mudduwa
The evaluation of kidney functions with the treatment of GA extracts is shown in Table 4. There was a significant increase in the concentrations of serum creatinine and BUN by 60% and 43% respectively, in rats of nephrotoxic control group compared to the normal healthy animals (p < 0.05). The treatment with the GA extract at the doses 100, 300 and 500 mg/kg markedly improved the kidney functions which was manifested as a significant reduction in creatinine and BUN by 18% 32%, 44% and 19%, 25%, 26% respectively for the three doses compared to the rats of ADR induced nephrotoxic control group (p < 0.05). Proteinuria is one of the early signs of kidney damage. The elevation of total protein concentration in urine over 70% in the nephrotoxic control group compared to the healthy control group signifies the kidney damage induced by ADR in experimental animals. The elevation of urinary protein due to glomerular and tubular injury resulted in subsequent reduction in serum concentrations of total protein (36%) and albumin (50%) in ADR induced nephrotoxic control rats. However, the standard drug, fosinopril was able to reduce proteinuria by 86% whereas the aqueous extract of GA stem bark at the three selected doses; 100, 300, 500 mg/kg reduced proteinuria by 48%, 74%, 73%, respectively. Further, serum total protein and albumin levels showed a dose dependent increase in GA-treated experimental animals. However, none of the experimental groups was able to restore the level of serum albumin within the short experimental period.
Fumarate exerted an antihypertensive effect and reduced kidney injury molecule (KIM)-1 expression in deoxycorticosterone acetate-salt hypertension
Published in Clinical and Experimental Hypertension, 2021
Osaze Edosuyi, Myung Choi, Ighodaro Igbe, Adebayo Oyekan
Proteinuria is indicative of renal damage resulting from hypertensive injury to the kidneys. The effect of fumarate on 24-hour protein excretion was evaluated in hypertensive rats placed on fumarate. As shown in Figure 3a, rats treated with DOCA-salt had a significant (p< .05, n = 8) increase in proteinuria that increased steadily over the duration of the study, when compared to control (n = 8). Fumarate reduced proteinuria, eliciting a 24% and 47% decrease on days 14 and 21, respectively, in DOCA-salt treated rats (p< .001, n = 8). KIM-1 is an indicator of progressive kidney injury that may result from hypertension. KIM-1 expression was increased in both the renal cortex (>100%, n = 4) and medulla (83%, n = 4) of DOCA-rats when compared to control (p< .001, n = 6) (Figure 3b). Fumarate reduced KIM-1 expression by 23% in the cortex (n = 4) and 19%, in the medulla (n = 3), when compared to DOCA group (p< .05, n = 6). The above data suggest that fumarate mitigates against hypertension-induced glomerular injury and appears to slow the progression of hypertensive renal nephropathy as indicated by the reduction in KIM-1 expression which may be indicative of reno-protective effects of TCA cycle products.
Preoperative proteinuria may be a risk factor for postoperative acute kidney injury：a meta-analysis
Published in Renal Failure, 2021
Dan-Dan Huang, Yuan-Yuan Li, Zhe Fan, Yong-Gui Wu
Proteinuria is a common clinical manifestation of chronic kidney disease, as well as its relationship with AKI has also been confirmed by more and more studies. The pathophysiological explanation of the association between proteinuria independent of baseline glomerular filtration rate (GFR) and risk factors of primary diseases, especially the existence of AKI by hypertension or diabetes mellitus (DM). The first possibility is that proteinuria is thought to be caused by acute kidney infection or immune inflammation. Secondly, the possibility is that proteinuria can lead to hypoalbuminemia, and then the decrease of inflation pressure caused by hypoalbuminemia lead to the contraction of intravascular volume and susceptibility to AKI. In our meta-analysis, the comprehensive results demonstrate that preoperative proteinuria is an independent risk factor for postoperative AKI.