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Chronic glomerulonephritis is related to focus infection. Odontogenic foci are frequently involved in glomerulonephritis. The relationship with the odontogenic focus infection can be demonstrated by the occurrence or aggravation of the symptoms of glomerulonephritis: proteinuria, haematuria, high blood pressure and oedema. Glomerular impairment in glomerulonephritis occurs together with inflammatory alterations of the tubulointerstitial compartment that can play an important part in the evolution of the disease. Tubular urinary markers can indicate the activation of this compartment during an infection of a focus, an odontogenic focus in our study.The paper aims at demonstrating the relationship between the odontogenic focus infection and tubulointerstitial lesions, assessed by a tubular urinary marker, N-acetyl beta-D glucosaminidase (NAG).We investigated the urinary N-acetyl beta-D glucosaminidase of 20 patients with chronic glomerulonephritis who presented odontogenic focus infections, comparing them with patients with chronic glomerulonephritis without odontogenic foci and of 20 controls, clinically healthy persons.Chronic glomerulonephritis patients with odontogenic focus infection presented clearly increased values as compared to clinically healthy control persons of urinary N-acetyl beta-D glucosaminidase.These patients underwent surgical intervention on the odontogenic focus under antibacterial prophylactic treatment. In 75% cases, the values of N-acetyl beta-D glucosaminidase diminished, indicating the favourable effect of the treatment of the odontogenic focus on the tubulointerstitial compartment in patients with chronic glomerulonephritis. In 25% cases this therapeutic treatment was associated with an increase of the values of urinary N-acetyl beta-D glucosaminidase, expressing its unfavourable effect on chronic glomerulonephritis.Urinary N-acetyl beta-D glucosaminidase indicated an etiopathogenetic relationship between the odontogenic focus and the tubulointerstitial compartment in chronic glomerulonephritis.

We present a case of idiopathic retroperitoneal fibrosis (RPF) in a female patient of 45 years, obese (BMI = 39 kg/sqm), hypertensive since 2005, with diabetes mellitus treated with diet and diabetes insipidus in whom, during a routine control, the following has been found: serum creatinine 1.74 mg/dl, and an inflammatory syndrome associated with fever. Spiral-CT (Multi-slice-Sensation 64) scan shows retroperitoneal fibrosis in relation with periaortitis that affects the thoracic and abdominal aorta. RPF is extending perirenally and at the level of the renal hilum with subsequent calyceal dilations (hydrocalycosis) associated with left renal artery stenosis. The particularity of the case is represented by the perirenal and intrarenal evolution of fibrosis with left renal artery stenosis with moderate impairment of renal function reversible under treatment with Tamoxifen. This case, with chronic periaortitis subsequent to an extended aortic atherosclerosis with retroperitoneal fibrosis can be representative for the pathogenic relationship between atherosclerosis and fibrosis.

Background: Thiazolidinediones represent a novel class of drugs that exert pleiotropic effects at various levels and lower blood glucose through reduction of insulin resistance in patients with type 2 diabetes mellitus., Main Purpose: The nephro- and neuroprotective effects of rosiglitazone vs. glimepiride were evaluated in normoalbuminuric patients with type 2 diabetes mellitus. The relevance of several biomarkers in the diagnosis of incipient diabetic nephropathy and cerebral microangiopathy was also assessed., Methods: A total of 34 normoalbuminuric patients with type 2 diabetes mellitus were enrolled in a 1-year open-label randomized controlled trial. Group A comprised 17 patients (7 men, 10 women, mean age 63 +/- 8.07 years) treated with rosiglitazone plus metformin; Group B comprised 17 patients (7 men, 10 women, mean age 63.2 +/- 7.19 years) treated with glimepiride plus metformin. All patients were assessed at initiation, at 6 months and by the end of the study concerning serum and urinary beta2-microglobulin, urinary a1-microglobulin, serum cystatin C, serum creatinine, glomerular filtration rate, C-reactive protein, fibrinogen, glycated hemoglobin, cholesterol, triglycerides, hemoglobin, and the urinary albumin/creatinine ratio (UACR). Cerebral hemodynamic parameters were also measured: pulsatility index and resistance index in the internal carotid artery and middle cerebral artery, and intima-media thickness in the common carotid artery., Results: At 1 year there were differences between groups A and B regarding serum cystatin C (P < 0.04), urinary beta2-microglobulin (P < 0.004), urinary a1-microglobulin (P < 0.0001), C-reactive protein (P < 0.0001), fibrinogen (P < 0.0001), serum creatinine (P < 0.0024), glomerular filtration rate (P < 0.0010), UACR (P < 0.0001), and the cerebral hemodynamic indices. The increase in a1- and beta2-microglobulin preceded the occurrence of microalbuminuria. UACR correlated with urinary a1- microglobulin (r = 0.4854), urinary beta2-microglobulin (r = 0.4867), and serum cystatin C (r = 0.3702). The cerebrovascular parameters improved in group A vs. group B and correlated with urinary beta2- and a1-microglobulin, C-reactive protein, fibrinogen, glomerular filtration rate, and duration of diabetes., Conclusion: Rosiglitazone demonstrated its nephro- and neuroprotective effects in normoalbuminuric patients with type 2 diabetes mellitus by the end of the follow-up period and these effects were beyond glycemic control. Urinary beta2- and a1-microglobulin are significant biomarkers for incipient diabetic nephropathy and diabetic cerebral microangiopathy. These biomarkers showed that proximal tubule dysfunction may develop before the stage of microalbuminuria.

Background: Cerebrovascular reactivity (CVR) is a hemodynamic parameter representing the increase in normal cerebral artery blood flow in response to a vasodilatory stimulus such as hypercapnia., Main Purpose: The aim of the study was to assess CVR using transcranial Doppler ultrasound and the breath-holding test (BHT) in normotensive patients with non-insulin-dependent diabetes mellitus (NIDDM). The cerebrovascular response to hypercapnia was evaluated in relation to risk factors for cerebral microangiopathy., Methods: The study was carried out in a group of 34 normotensive NIDDM patients and a group of 31 sex- and age-matched normal controls. The NIDDM group was subdivided into 21 patients with microangiopathic complications (Group A, 12 men, 9 women; mean age 58.77 +/- 8.91 years) and 13 patients with no such complications (Group B, 8 men, 5 women; mean age 56.34 +/- 9.83 years). The control group comprised 17 men and 14 women (Group C, mean age 58.43 +/- 6.31 years). Exclusion criteria were hypertension and past or present symptomatic cerebrovascular disease. The BHT consisted of spontaneous hypercapnia induced by holding the breath for 20 seconds. CVR was estimated in relation to the increase in the mean flow velocity (MFV) compared with the basal velocity in both middle cerebral arteries during hypercapnia., Results: In Group A, the CVR was significantly decreased in 71.42% of patients, whereas in Group B only 30.76% of patients presented with mildly to moderately impaired CVR. Predictors for impaired % increase in the MFV during the BHT demonstrated by univariate regression analysis were: duration of diabetes (r = 0.802; P < 0.0001), fibrinogen (r = 0.574; P < 0.0001), C-reactive protein (r = 0.525; P < 0.001), proteinuria (r = 0.924; P < 0.0001) and serum creatinine (r = 0.969; P < 0.0001). Multivariate regression analysis showed as predictors: duration of diabetes (P < 0.0001), proteinuria (P < 0.0001) and serum creatinine (P < 0.0001)., Conclusion: CVR is impaired in normotensive NIDDM patients. These cerebral hemodynamic changes correlate significantly with the duration of DM, parameters of inflammation, proteinuria and serum creatinine.