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In patients with resistant hypertension (RH) we investigated the importance of urinary neutrophil gelatinase-associ- ated lipocalin (uNGAL- a chemiluminescent microparticle immunoassay (CMIA) method became using (Abbott Diag- nostics) for the measurement of NGAL in urine samples) and incidence of chronic kidney disease using the Modification of Diet in Renal Disease Study (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations in estimating glomerular filtration rate (eGFR) based on standardised serum creatinine method traceable to isotope di- lution mass spectrometry (IDMS) method. It would have been difficult to predict that levels of these biomarker would per- form better organ damage than traditional measurements of kidney function such as standardised serum creatinine, MDRD, or CKD-EPI equations in special population such as RH. Serum creatinine concentrations were measured in 50 patients (24M:26F, from RH Registar in Clinical Hospital Merkur) by the kinetic Jaffe method. There were no significant differences between the GFR values derived by MDRD and CKD-EPI equations in the group of patients with RH. 62% of patients have eGFR >60 mL/min/1.73 m 2 , while a 38% of patients have eGFR <60 mL/min/1.73 m 2 . The measurement of NGAL in urine samples of 40 patients with RH showed no difference and seems to be of no use in furthere determination of renal impairement. Higher value of uNGAL in some resistant hypertension patients could have link in the repair stage after AKI and would reveal pathways that could link AKI and CKD.

Hyperfiltration has been documented in type 1 diabetes and may contribute to the high risk for development of albuminuria and progression of nephropathy. However, recent studies suggest that the risk of progression to albuminuria in type 1 diabetes was not increased by hyperfiltration. We investigated associations of estimated glomerular filtration rate (eGFR) and urinary albumin excretion rate (UAE) in normoalbuminuric type 1 diabetic patients. Study included 313 normoalbuminuric patients with type 1 diabetes, none showed signs of adrenal, renal, or cardiovascular diseases. GFR was estimated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula. Glomerular hyperfiltration was defined as eGFR ³ 125 mL min–1 1.73 m–2. Renal hyperfiltration was present in 12% of the study group. Subjects with eGFR ³ 125 mL min–1 1.73 m–2 were younger, had shorter duration of diabetes, lower levels of total and LDL cholesterol, and higher HbA1c than subjects with an eGFR below 125 mL min–1 1.73 m–2. Type 1 diabetic patients with hyperfiltration also had significantly lower UAE. In a multiple logistic regression analysis, higher eGFR was associated with lower UAE. Our results indicate that normoalbuminuric type 1 diabetic patients with hyperfiltration have lower UAE than those with renal function in the normal range. Together with other recent studies this may suggest that creatinine-based estimates of GFR indicating hyperfiltration is not associated with higher UAE and subsequent development of microalbuminuria.

Although insulin resistance is usually associated with the development of type 2 diabetes, it can also be a feature of patients with type 1 diabetes. Insulin resistance has been documented in type 1 diabetes and may contribute to the high risk of cardiovascular disease in this population. To investigate the relationship of insulin resistance with metabolic and inflammatory parameters we divided 304 patients according to median estimated glucose disposal rate (eGDR =9.72 mgkg-1min-1) into lower (n=153) and higher (n=151) insulin sensitivity groups. Patients with lower insulin sensitivity had higher levels of serum lipids (except for HDL cholesterol), duration of diabetes, daily insulin dose, white blood cell count, C-reactive protein, homocysteine and ferritin. Spearman correlation analysis showed significant associations between individual components of insulin resistance and various metabolic and inflammatory parameters. Multiple logistic regression models found significant association of age, sex, duration of diabetes, serum lipids, daily insulin dose, white blood cell count and ferritin with progression to insulin resistance. The presence of insulin resistance indicates a greater risk of micro- and macrovascular disease and health care professionals need to be alerted that this subset of individuals with type 1 diabetes will require stringent control of hypertension, glycemia and serum lipids., Inzulinska rezistencija u tipu 1 šećerne bolesti dokazano doprinosi povećanom riziku razvoja kardiovaskularne bolesti. U ovoj studiji istraživana je razina inzulinske osjetljivosti koristeći kliničke parametre (eGDR ) u bolesnika sa šećernom bolešću tipa 1 i istraživan je odnos razine inzulinske osjetljivosti s metaboličkim i upalnim parametrima. Od 304 bolesnika uključena u studiju njih 153 imalo je nižu inzulinsku osjetljivost (eGDR <9.72 mgkg-1min-1), a 151 bolesnik imao je višu inzulinsku osjetljivost (eGDR ≥9.72 mgkg-1min-1). Bolesnici s nižom razinom inzulinske osjetljivosti imali su značajno više vrijednosti lipida u serumu (osim HDL kolesterola), indeks tjelesne težine, trajanje šećerne bolesti te upalne parametre, a svi navedeni čimbenici zajedno i pojedinačno doprinose razvoju mikro- i makrovaskularnih komplikacija u osoba oboljelih od šećerne bolesti tipa 1. Multiplom logističkom regresijom dokazano je da na razvoj inzulinske rezistencije u šećernoj bolesti tipa 1 utječu spol, godine života, trajanje šećerne bolesti, serumski lipidi, glikemija natašte, dnevna doza apliciranog inzulina i leukociti. Inzulinska rezistencija u tipu 1 šećerne bolesti doprinosi povećanom riziku razvoja mikro- i makrovaskularnih komplikacija, a ti pojedinci unutar skupine bolesnika sa šećernom bolešću tipa 1 zahtijevaju strožu kontrolu povišenog krvnog tlaka, glikemije i serumskih lipida.

Although metabolic syndrome was not extensively studied in type 1 diabetes, higher insulin resistance, the core feature of the syndrome was found to be associated with increased risk of developing microvascular complications. As diabetic nephropathy may progress to advanced lesion before microalbuminuria appears, we investigated the association of the metabolic syndrome and estimated glucose disposal rate (eGDR) with urinary albumin excretion (UAE), retinopathy and neuropathy in normoalbuminuric type 1 diabetic patients. Two hundred and 98 patients (UAE <30 mg / 24 h at three occasions) were divided according to the IDF metabolic syndrome; eGDR (mg kg–1 min–1) was calculated: 24.31– (12.22 ´ WHR) – (3.29 ´ HT) – (0.57 ´ HbA1c), (WHR=waist-to-hip ratio, HT=hypertension). Patients with (n=99) compared to those without metabolic syndrome (N=199) showed higher UAE (15.96±9.10; 13.48±8.36 mg / 24 h), C-reactive protein (2.39±4.09;1.12±2.03 mg/L), prevalence of retinopathy (70.7;55.27%) and polyneuropathy (80.8; 68.3%), and lower eGDR (5.75±1.74; 8.96±1.9), (p>0.05). In patients with high-normal UAE, retinopathy and polyneuropathy eGDR was significantly lower compared with patients with low-normal UAE, and without retinopathy and polyneuropathy. In multiple regression analysis UAE and retinopathy were associated with diabetes duration (b= –0.20, b= -0.62), eGDR (b= – 0.106; b= –0.041), metabolic syndrome (b=0.49, b=0.28), (p>0.05). In type 1 diabetic patients insulin resistance and IDF defined metabolic syndrome are associated with high-normal UAE, retinopathy and polyneuropathy. The predictive value of the metabolic syndrome for development of microalbuminuria and retinopathy needs to be assessed in further follow-up studies.

Insulin resistance has been documented in type 1 diabetes and may contribute to the high risk for cardiovascular disease in this population and progression of nephropathy. We investigated associations of renal parameters, including urinary albumin excretion rate (UAE), serum creatinine and creatinine clearance, with surrogate measure of insulin sensitivity calculated using a formula derived from euglycemic-hyperinsulinemic clamp studies (estimated glucose disposal rate, eGDR). Study included 353 patients with type 1 diabetes, none showed signs of adrenal, thyroid, renal, or cardiovascular diseases. Insulin sensitivity was measured with eGDR calculated with the equation: 24.31–(12.22´WHR)– (3.29´HT)–(0.57´HbA1c). The units were mgkg–1min–1; WHR=waist to hip ratio; HT=hypertension. Correlations and logistic regression analysis were performed to identify relationships between renal parameters and eGDR, individual components of insulin resistance and risk of insulin resistance. UAE and serum creatinine significantly correlated with insulin resistance measured by eGDR (r=–0.13, and –0.17, all p<0.05), and its components disorders, WHR and HbA1c. After stratifying patients in quartiles of eGDR, those in the upper quartile of the eGDR had significantly reduced levels of UAE and serum creatinine, compared to subjects in lowest quartile. In a logistic regression analysis risk for development of insulin resistance in our subjects were independently predicted only by UAE (odds ratio=1.01, p<0.01). Our results provide evidence of associations between insulin resistance and its components disorders with renal parameters, such as UAE and serum creatinine. Insulin resistance, measured with eGDR, predicts the increment in UAE in subjects with type 1 diabetes. Since progression to microalbuminuria is likely to occur in majority of diabetic patients, there is a need to further explore the role of risk factors such as insulin resistance.