scholarly journals Diabetológia és szervátültetés

2018 ◽  
Vol 159 (46) ◽  
pp. 1930-1939 ◽  
Author(s):  
László Wagner ◽  
István Wittmann ◽  
László Piros ◽  
Réka P. Szabó ◽  
Péter Szakály

Abstract: Diabetes increases the risk of different kidney diseases. The most important is diabetic nephropathy, however, ischemic kidney disease, chronic pyleonephritis and papilla necrosis may also develop. The prognosis of diabetic nephropathy has improved recently, however, it is still the primary cause of dialysis and transplantation. Cardiovascular diseases predict mostly mortality in diabetic patients, however, cerebrovascular insults and peripheral obstructive arterial diseases necessitating lower limb amputations are also important. Diabetic retinopathy is almost always present with diabetic nephropathy. Diabetic neuropathy may also develop, furthermore vascular complications often combine. All these urge complex workup, follow-up and early treatment. If transplantation is indicated, preemptive operation should be preferred, and living donation shows the best outcomes. Different forms of carbohydrate disorder may occur after transplantation: new-onset diabetes or diabetes known before transplantation may progress. Renal transplantation with pancreas transplantation may be indicated in type 1 diabetes with end-stage diabetic nephropathy, most often simultaneously. This may result in normoglycemia and insulin-independence and the progression of other complications may also halt. Transplant associated hyperglycemia occurs in most of the patients early, however, it is often transitory. Despite stabilization of the patient and of the immunosuppressive therapy, about one third of the patients may develop posttransplant diabetes. Insulin secretion disorder is the primary cause, but insulin resistance is also needed. Insulin administration may help, however, other antidiabetics can also be useful. Carbohydrate metabolism should be checked in both cadaveric and living donors. The authors make an attempt to summarize the above conditions with Hungarian relevance as well. Orv Hetil. 2018; 159(46): 1930–1939.

2017 ◽  
Vol 5 (2) ◽  
pp. 188-192 ◽  
Author(s):  
Soha M. Abd El Dayem ◽  
Abo El Magd El Bohy ◽  
Mona Hamed ◽  
Solaf Ahmed

AIM: To evaluate intrarenal resistivity index (RI) and different biomarkers of diabetic nephropathy (DN) with clinical signs of DN and its progression over time as early detection of DN.PATIENTS AND METHODS: This longitudinal study included 48 type 1 diabetic patients who were studied at baseline and after three years. A blood sample was taken for assessment of glycosylated haemoglobin (HbA1), lipid profile and a urine sample was taken for assessment of albumin/creatinine ratio, Neutrophil gelatinase-associated lipocalin (NGAL), liver-type fatty acid binding protein (L-FABP) and kidney injury molecule-1 (Kim-1) at baseline and after three years. Forty diabetic patients did renal Doppler at baseline & after three years.RESULTS: HbA1, waist/hip ratio, albumin/creatinine ratio, lipid profile, NGAL, KIM-1, L-FABP and resistivity index (RI) were significantly increased in follow-up. Twenty patients (41.7%) showed progression to albuminuria. RI showed a significant increase in follow-up study. ROC curve showed that RI and NGAL had the highest sensitivity (100%), followed by L-FABP (90%) and lastly KIM-1 (63.6%) in the prediction of DN.CONCLUSION: High RI, NGAL, KIM-1 & L-FABP can be considered as early markers of diabetic nephropathy in type 1 diabetics and are associated with its progression over time, independent of albuminuria.


2021 ◽  
Vol 22 (18) ◽  
pp. 9985
Author(s):  
Amit K. Maiti

Diabetic Nephropathy (DN) is a debilitating consequence of both Type 1 and Type 2 diabetes affecting the kidney and renal tubules leading to End Stage Renal Disease (ESRD). As diabetes is a world epidemic and almost half of diabetic patients develop DN in their lifetime, a large group of people is affected. Due to the complex nature of the disease, current diagnosis and treatment are not adequate to halt disease progression or provide an effective cure. DN is now considered a manifestation of inflammation where inflammatory molecules regulate most of the renal physiology. Recent advances in genetics and genomic technology have identified numerous susceptibility genes that are associated with DN, many of which have inflammatory functions. Based on their role in DN, we will discuss the current aspects of developing biomarkers and molecular therapy for advancing precision medicine.


2020 ◽  
Author(s):  
Aila J. Ahola ◽  
Valma Harjutsalo ◽  
Carol Forsblom ◽  
François Pouwer ◽  
Per-Henrik Groop ◽  
...  

OBJECTIVE To investigate the relationship between depression and diabetic nephropathy progression in type 1 diabetes. <p>RESEARCH DESIGN AND METHODS Data from 3730 participants without end-stage renal disease at baseline, participating in the Finnish Diabetic Nephropathy Study, were included. Depression was assessed in three ways. Depression diagnoses were obtained from the Finnish Care Register for Health Care. Antidepressant agent purchase data were obtained from the Drug Prescription Register. Symptoms of depression were assessed using the Beck Depression Inventory (BDI). Based on their urinary albumin excretion rate (AER) participants were classified into those with normal AER, microalbuminuria, and macroalbuminuria. Progression from normal AER to either microalbuminuria, macroalbuminuria, or end-stage renal disease; or from microalbuminuria to macroalbuminuria or ESRD; or from macroalbuminuria to ESRD, during the follow-up period was investigated.</p> <p>RESULTS Over a mean follow-up period of 9.6 years, renal status deteriorated in 18.4% of the participants. Diagnosed depression and antidepressant purchases before baseline were associated with 53% and 32% increased risk of diabetic nephropathy progression, respectively. Diagnosed depression assessed during follow-up remained associated with increased risk of disease progression (32%). BDI-derived symptoms of depression showed no association with the progression, but the total number of antidepressant purchases modestly reduced the risk [0.989 (0.982–0.997), P=0.008]. Dividing the sample based on median age, the observations followed those seen in the whole group. However, symptoms of depression additionally predicted progression in those ≤36.5 years.</p> <p>CONCLUSIONS<b> </b>Diagnosed depression and antidepressant purchases are associated with the progression of diabetic nephropathy in type 1 diabetes. Whether successful treatment of depression reduces the risk needs to be determined. </p>


2020 ◽  
Author(s):  
Aila J. Ahola ◽  
Valma Harjutsalo ◽  
Carol Forsblom ◽  
François Pouwer ◽  
Per-Henrik Groop ◽  
...  

OBJECTIVE To investigate the relationship between depression and diabetic nephropathy progression in type 1 diabetes. <p>RESEARCH DESIGN AND METHODS Data from 3730 participants without end-stage renal disease at baseline, participating in the Finnish Diabetic Nephropathy Study, were included. Depression was assessed in three ways. Depression diagnoses were obtained from the Finnish Care Register for Health Care. Antidepressant agent purchase data were obtained from the Drug Prescription Register. Symptoms of depression were assessed using the Beck Depression Inventory (BDI). Based on their urinary albumin excretion rate (AER) participants were classified into those with normal AER, microalbuminuria, and macroalbuminuria. Progression from normal AER to either microalbuminuria, macroalbuminuria, or end-stage renal disease; or from microalbuminuria to macroalbuminuria or ESRD; or from macroalbuminuria to ESRD, during the follow-up period was investigated.</p> <p>RESULTS Over a mean follow-up period of 9.6 years, renal status deteriorated in 18.4% of the participants. Diagnosed depression and antidepressant purchases before baseline were associated with 53% and 32% increased risk of diabetic nephropathy progression, respectively. Diagnosed depression assessed during follow-up remained associated with increased risk of disease progression (32%). BDI-derived symptoms of depression showed no association with the progression, but the total number of antidepressant purchases modestly reduced the risk [0.989 (0.982–0.997), P=0.008]. Dividing the sample based on median age, the observations followed those seen in the whole group. However, symptoms of depression additionally predicted progression in those ≤36.5 years.</p> <p>CONCLUSIONS<b> </b>Diagnosed depression and antidepressant purchases are associated with the progression of diabetic nephropathy in type 1 diabetes. Whether successful treatment of depression reduces the risk needs to be determined. </p>


2020 ◽  
Vol 27 (11) ◽  
pp. 1744-1763 ◽  
Author(s):  
Stefano Menini ◽  
Carla Iacobini ◽  
Claudia Blasetti Fantauzzi ◽  
Giuseppe Pugliese

Vascular complications are among the most serious manifestations of diabetes. Atherosclerosis is the main cause of reduced life quality and expectancy in diabetics, whereas diabetic nephropathy and retinopathy are the most common causes of end-stage renal disease and blindness. An effective therapeutic approach to prevent vascular complications should counteract the mechanisms of injury. Among them, the toxic effects of Advanced Glycation (AGEs) and Lipoxidation (ALEs) end-products are well-recognized contributors to these sequelae. L-carnosine (β-alanyl-Lhistidine) acts as a quencher of the AGE/ALE precursors Reactive Carbonyl Species (RCS), which are highly reactive aldehydes derived from oxidative and non-oxidative modifications of sugars and lipids. Consistently, L-carnosine was found to be effective in several disease models in which glyco/lipoxidation plays a central pathogenic role. Unfortunately, in humans, L-carnosine is rapidly inactivated by serum carnosinase. Therefore, the search for carnosinase-resistant derivatives of Lcarnosine represents a suitable strategy against carbonyl stress-dependent disorders, particularly diabetic vascular complications. In this review, we present and discuss available data on the efficacy of L-carnosine and its derivatives in preventing vascular complications in rodent models of diabetes and metabolic syndrome. We also discuss genetic findings providing evidence for the involvement of the carnosinase/L-carnosine system in the risk of developing diabetic nephropathy and for preferring the use of carnosinase-resistant compounds in human disease. The availability of therapeutic strategies capable to prevent both long-term glucose toxicity, resulting from insufficient glucoselowering therapy, and lipotoxicity may help reduce the clinical and economic burden of vascular complications of diabetes and related metabolic disorders.


Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 457
Author(s):  
Kyeong-Seok Kim ◽  
Jin-Sol Lee ◽  
Jae-Hyeon Park ◽  
Eun-Young Lee ◽  
Jong-Seok Moon ◽  
...  

Diabetic nephropathy (DN) is one of the most common complications of diabetes mellitus. After development of DN, patients will progress to end-stage renal disease, which is associated with high morbidity and mortality. Here, we developed early-stage diagnostic biomarkers to detect DN as a strategy for DN intervention. For the DN model, Zucker diabetic fatty rats were used for DN phenotyping. The results revealed that DN rats showed significantly increased blood glucose, blood urea nitrogen (BUN), and serum creatinine levels, accompanied by severe kidney injury, fibrosis and microstructural changes. In addition, DN rats showed significantly increased urinary excretion of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL). Transcriptome analysis revealed that new DN biomarkers, such as complementary component 4b (C4b), complementary factor D (CFD), C-X-C motif chemokine receptor 6 (CXCR6), and leukemia inhibitory factor (LIF) were identified. Furthermore, they were found in the urine of patients with DN. Since these biomarkers were detected in the urine and kidney of DN rats and urine of diabetic patients, the selected markers could be used as early diagnosis biomarkers for chronic diabetic nephropathy.


Diabetologia ◽  
2008 ◽  
Vol 52 (1) ◽  
pp. 46-49 ◽  
Author(s):  
K. J. Schjoedt ◽  
A. S. Astrup ◽  
F. Persson ◽  
E. Frandsen ◽  
F. Boomsma ◽  
...  

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