Incidence of SARS-COV-2 infection among swimming athletes: data from real life in Apulia (Italy), July 2020/August 2021.

Background: As other indoor sports facilities, swimming pools were closed in Italy from March to May 2020 and from October 2020 to July 2021 due to the outbreak of the COVID-19 pandemic; access to these facilities was restricted to athletes of national relevance. This decision was based on "precautionary principles" and without evidence of a high risk of SARS-COV-2 circulation among swimming pools' attendants. The aim of this paper is to describe the pattern of SARS-COV-2 circulation among swimming athletes in Apulia (Southern Italy). Study design: The study aims to investigate the hypothesis that attending a pool increases the risk of SARS-COV-2 infection. The outcome measure is the incidence of SARS-COV-2 infection among swimming athletes compared with the general population. Methods: This is a retrospective cross-sectional study carried out in Apulia, Southern Italy. The study was performed through the analysis of both the database of the Italian Swimming Federation and the SARS-COV-2 infections in Apulia Region, from July 2020 to August 2021. Results: Among 2,939 federally licensed athletes, 221 had an history of SARS-COV-2 infection from July 2020 to August 2021, with an incidence of 75.2 /1,000. In the general Apulian population, during the same time span, the incidence of SARS-COV-2 infection was 67.3/1,000 and - considering the incidence rate ratio - there is no difference between the two populations (IRR=1.1; 95% CI=0.9-1.3; p>0.05). Conclusions: The incidence of SARS-COV-2 infection in Apulian swimmers showed no significant differences with the general population.

Which physical activity in patients affected by hypoparathyroidism? A review of the literature and practical recommendations.

BACKGROUND: Hypoparathyroidism (HypoP) is a rare endocrine condition characterized by hypocalcaemia and hyperphosphatemia, as a consequence of absent or improperly low parathyroid hormone (PTH) levels. Patients affected by HypoP have a clinical condition often characterized by paresthesias and muscle spasms, as well as long-term consequences as nephrolithiasis, extraskeletal calcification, and fractures. In the literature, likely due to these symptoms, few data exist regarding the appropriate physical activity (PA) in subjects suffering from HypoP. PURPOSE: This review evaluates the literature on exercise-based approaches to the management of individuals affected by HypoP and evaluates: (1) the effects of physical exercise on muscle cramps and other clinical symptoms; (2) the effects of exercise on PTH and calcium level; (3) the most suitable clinical exercise testing; and (4) the most suitable exercise combination. METHODS AND RESULTS: A systematic search was conducted using the databases MEDLINE, Google Scholar using "hypoparathyroidism AND Physical Activity", "Training AND hypoparathyroidism", "Exercise AND muscle cramps", "Exercise AND Fatigue" as keywords. In addition, references list from the included articles were searched and cross-checked to identify any further potentially eligible studies. A total of 50 manuscripts were found among which 39 manuscripts were selected. A few clinical studies have been performed in HypoP patients to evaluate PA training protocols. CONCLUSION: Although further research is needed to draw solid conclusions regarding best PA protocols in subjects affected by HypoP, a PA protocol has been proposed within the manuscript to encourage patients to attempt exercise to improve their clinical conditions and their quality of life.

Daily pilates exercise or inactivity for patients with low back pain: a clinical prospective observational study.

BACKGROUND: Studies have shown the effectiveness of a few weekly pilates sessions as helping to reduce lower back pain (LBP). However many patients fear that physical activity can actually make the pain and disability worse. DESIGN: We carried out this observational prospective clinical study to look at the effects that taking part in daily pilates has one on side and on the other the effects of LBP management without physical exercise. SETTING: The volunteers who participated in this study were recruited from among some local cultural associations. POPULATION: Patients affected by LBP were evaluated. METHODS: The subjects were 60 volunteers (27 males and 33 females) with a mean age of 51.2 years who had chronic low back pain (CLBP). They were allocated to pilates group (N.=30) or inactivity control group (N.=30). The pilates group performed one-hour lesson of pilates exercise, 5 lessons per week during the following 6 months. The inactivity group continued with their normal daily activities. The Roland-Morris Disability, the Oswestry, the SF-36 and the Spinal Functional Sort Questionaries of all subjects were measured at the baseline (T1) and at 6 months (T2). RESULTS: At T2 improvements were observed in the pilates group with increases in physical and social functioning, general health and vitality (P<0.05) and decreases in disability and pain (P<0.05). The inactivity group showed worsening in the same measures at T2. CONCLUSION: We found an important improvement of pain, disability and physical and psychological perception of health in individuals who did the daily sessions of pilates. CLINICAL REHABILITATION IMPACT: Some authors underlined the possible risk of a lack of adherence to an exercise program at home. This study suggests that a daily pilates program is effective for the management of CLBP. On the other hand, the inactivity contributes to further worsening, inducing a vicious cycle in which pain and physical activity intolerance follow each other.

Innate immunity, through late complement components activation, contributes to the development of early vascular inflammation and morphologic alterations in experimental diabetes.

OBJECTIVE: To verify if innate immunity, and namely the assembly of terminal complement complex (TCC) could be involved in the development of early diabetic vascular damage. METHODS AND RESULTS: At first in 2 groups of diabetic or non-diabetic Wistar rats the occurrence of basal or stimulated stable adherence to the endothelial layer and extravasation of circulating fluorescently-labelled leukocytes was assessed by using an in vivo videomicroscopy technique. In a second part of the study, the development of vascular damage in short term diabetes was studied in the genetically C6 deficient rats of the PVG strain, and compared with those observed in the wild-type C6 sufficient animals. Here, the analysis of mesentery vascular expression of mRNA for vascular cell adhesion molecule (VCAM)-1, transforming growth factor-ß (TGF-ß), connective tissue growth factor (CTGF), and platelet-derived growth factor (PDGF), the evaluation of intravascular protein levels of VCAM-1, TGF-ß, CTGF, proliferative cell nuclear antigen (PCNA), as well as the assessment of structural changes and Complement components deposition at the mesentery arterial vascular wall were also performed. CONCLUSIONS: Leukocyte trafficking, mesentery arteries hypertrophy, extracellular matrix deposition, local vascular gene and protein expression of VCAM-1, TGF-ß, CTGF and PCNA, as well as PGDF gene expression were all increased by short term diabetes, but all significantly reduced in the C6 deficient diabetic animals, thus suggesting an active role for TCC in the development of vascular inflammation in the early phases of experimental diabetes.

Study on the possible role of the -174G>C IL-6 promoter polymorphism in predicting response to rituximab in rheumatoid arthritis.

OBJECTIVE: Identification of genetic biomarkers of response to biologics in rheumatoid arthritis (RA) is a relevant issue. The -174G>C interleukin-6 (IL-6) promoter polymorphism was investigated in RA patients treated with rituximab (RTX), being IL-6 a key cytokine for B cell survival and proliferation, thus possibly implicated in rituximab efficacy. METHODS: The study was conducted in a real-life retrospective cohort of 142 unselected RA patients (120F/22M) treated with RTX and referred to 7 rheumatologic centres in the north of Italy. One hundred and thirteen (79.6%) patients were rheumatoid factor (RF)-positive and 112 (78.9%) were anti-CCP antibodies positive. The response to therapy was evaluated at the end of the sixth month after the first RTX infusion, by using both the EULAR criteria (DAS28) and the ACR criteria. The IL-6 -174G>C promoter polymorphism was analyzed by RFLP following previously reported methods. RESULTS: Lack of response to RTX at month +6 by EULAR criteria was more prevalent in RA patients with the IL-6 -174 CC genotypes (9/21, 42.8%), than in the GC/GG patients (23/121, 19.0%) (OR 3.196, 95% CI=1.204-8.485; p=0.0234). Similar results were found when evaluating the response by ACR criteria. No differences were found in RA duration, baseline DAS28, baseline HAQ, RF status, anti-CCP status according to the different IL-6 -174 genotypes. CONCLUSION: IL-6 promoter genotyping may be useful to better plan treatment with RTX in RA. Larger replication studies are in course to confirm these preliminary results.

Parathyroid cancer as rare cause of primary hyperparathyroidism. Case report and review of the literature.

Primary hyperparathyroidism (PHPT) due to parathyroid carcinoma is rare, and affects more frequently women in their 4th-5th decades of life. Parathyroid cancer (PC) accounts for 0.5% up to 5% of the patients with primary hyperparathyroidism (PHPT). Diagnosis of PC is not easy, and a lot of patients with PHPT receive no pre-operative or intra-operative diagnosis of malignancy. Most of PC are hyperfunctioning, with marked serum PTH levels, and symptoms occurs more frequently than in benign disease. We report the case of a 52 years old woman that underwent a single parathyroidectomy for hyperfunctioning gland. Histological examination revealed carcinoma. Parathyroid carcinoma is rare and surgery represent the only curative approach, although there can be a local recurrence of the disease. A pre-operative diagnosis is not easy, and many features that suggest the diagnosis of malignancy are controversial. According to the literature, we think that the cure of the parathyroid cancer is difficult to achieve. After two years of follow- up, our patient is in good conditions and has no evidence of disease. A careful follow up is of primary importance to diagnose the local recurrence of disease and perform a second surgical treatment, to achieve the control of hypercalcemia, which causes severe metabolic alterations and visceral lesions until the death.

Feto-maternal immune interaction at the placental level.

A special interaction is established during pregnancy between the maternal immune system and fetal cells to allow the survival and the normal growth of the fetus. Fetal cells expressing paternal alloantigens are not recognized as foreign by the mother because of an efficient anatomic barrier and a local immunosuppression determined by the interplay of locally produced cytokines, biologically active molecules and hormones. A special balance between TH1 and TH2 lymphocytes has also been observed at the feto-maternal barrier that contribute to control the immune response at this level. An important role is played by trophoblast cells that act as a physical barrier forming a continuous layer and exert immunomodulatory function. Trophoblast cells have also been shown to express regulators of the complement system and to downregulate the expression of HLA antigens. Dysfunction of these cells leads to morphological and functional alterations of the feto-maternal barrier as well as to hormonal and immune imbalance and may contribute to the development of pathologic conditions of pregnancy, such as recurrent spontaneous abortions. Efforts are still needed to better understand the physiology of the feto-maternal interaction and the pathogenetic mechanisms responsible for tissue damage in pathologic conditions of pregnancy.

Fluvastatin treatment inhibits leucocyte adhesion and extravasation in models of complement-mediated acute inflammation.

Complement activation plays a relevant role in the development of tissue damage under inflammatory conditions, and clinical and experimental observations emphasize its contribution to inflammatory vasculitides. Statins have recently been shown to reduce cardiovascular morbidity independently of plasma cholesterol lowering and in vitro studies support a direct anti-inflammatory action of these drugs. The aim of this study was to verify the in vivo effect of fluvastatin on complement-mediated acute peritoneal inflammation. The effect of oral treatment with fluvastatin was investigated in normo-cholesterolaemic rats that received intraperitoneal injection of either yeast-activated rat serum (Y-act RS) or lipopolysaccharide to induce peritoneal inflammation monitored by the number of PMN recruited in peritoneal fluid washes. In addition, vascular adherence and extravasation of leucocytes were evaluated by direct videomicroscopy examination on mesentery postcapillary venules topically exposed to Y-act RS. The number of PMN in the peritoneal washes of rats treated with fluvastatin was 38% lower than that of untreated animals (P < 0.05) 12 h after LPS injection, and was even lower (56%) in rats treated with Y-act RS already 8 h after injection (P < 0.02). Firm adhesion to endothelium and extravasation of leucocytes evaluated under direct videomicroscopy observation were significantly inhibited in fluvastatin treated rats (77% and 72%, respectively; P < 0.01), 120 min after treatment with Y-act RS. Our results demonstrate that fluvastatin inhibits in vivo complement-dependent acute peritoneal inflammation and suggest a role for statins in preventing the inflammatory flares usually associated with complement activation in chronic diseases, such as SLE or rheumatoid arthritis.

Abrupt occurrence of high fever and rash in a patient treated with sulphasalazine for psoriatic arthritis.

We report a singular clinical condition observed following a short duration treatment with sulphasalazine (SSZ) in a 64-year-old woman affected by psoriatic arthritis. Two weeks after starting treatment, a high degree, subcontinuous fever occurred, together with systemic discomfort, fatigue, headache, and ultimately a moderate wakefulness impairment. Upon admission to the hospital, a malar rash became evident. Modest notes of hepatotoxicity were also evident. All of the symptoms suddenly resolved after SSZ withdrawal. The markers of hepatitis become negative just 2 months later. It is interesting to note that after dismissal, in order to counteract the severe arthritic conditions and the presence of a type 2 diabetes, a combined therapy with methotrexate and cyclosporin had to be used, with no renal or hepatic side effects and remarkable therapeutic effects. No markers of autoimmunity were found in this patient. The chronology and the clinical events here described may confirm the hypothesis of a idiosyncratic reaction to SSZ, closely resembling a rare, sometimes irreversible, condition known as "the 3 week sulphasalazine syndrome".

Mechanics of the carotid artery wall and baroreflex sensitivity after acute ethanol administration in young healthy volunteers.

The effects of ethanol administered orally (300 mg/kg in 250 ml of water) or intravenously (7.5 mg.min(-1).kg(-1) in 250 ml of saline over 40 min) on common carotid haemodynamics, wall mechanics and baroreflex sensitivity were compared with the effects of the intravenous infusion of 250 ml of saline. Ethanol or saline was administered to 10 healthy volunteers after 30 min of supine rest, and measurements were obtained 40 min (median; range 34-46 min) after administration. After ethanol administration, the plasma alcohol level rose from 0 to 0.3+/-0.07 g/l. Mean arterial blood pressure had risen slightly at 20 min, but was normalized by 40 min, the time at which the haemodynamic study was performed. Heart rate decreased after infusion of either saline or alcohol, but was unchanged after oral ethanol administration. Both oral and intravenous ethanol administration were associated with significant decreases in baroreflex sensitivity, carotid shear stress and blood velocity, compared with resting values, while the mean carotid artery diameter was increased, and blood viscosity and mean blood flow were unchanged. No changes were observed in these parameters after saline administration. Ethanol, administered either intravenously or orally, increased the stiffness of the carotid artery and decreased the pulsatility (systo-diastolic changes) of its diameter. A direct, statistically significant correlation was found between the decrease in shear stress and the decrease in baroreflex heart rate control sensitivity after both modes of alcohol administration, while no such correlation was found between the increase in the Peterson elastic modulus and the decrease in carotid diameter pulsatility on the one hand or the decrease in baroreflex sensitivity on the other. In conclusion, reduced shear stress associated with vasodilatation of the carotid artery wall may contribute to the decrease in baroreflex sensitivity observed after acute ethanol administration.

Detection of mRNA for the terminal complement components C5, C6, C8 and C9 in human umbilical vein endothelial cells in vitro.

Human umbilical vein endothelial cells (HUVEC) have previously been shown to synthesize the functional terminal pathway of complement based on the detection by radioimmunoassay of the terminal complement complex (TCC) on coincubated agarose beads. In addition, C7 secretion by these cells in amounts comparable to C3, as well as C7 mRNA, has recently been demonstrated. However, it has not been possible to detect C5-6 and C8 in the fluid phase, and only trace amounts of soluble C9. Against this background we examined whether mRNA for the remaining terminal complement factors was present in HUVEC. By the use of reverse transcription (RT)-polymerase chain reaction (PCR) and Northern blot the presence of mRNA for complement factors C5, C6, C8 and C9 was demonstrated.

Haemoconcentration, shear-stress increase and carotid artery diameter regulation after furosemide administration in older hypertensives.

The aim of the present study was to determine whether changes of carotid wall shear stress induced by changes in blood viscosity after diuretic administration cause carotid arterial dilatation in elderly hypertensives, as reported in the cat. Arterial wall shear rate (ultrasound technique, profilmeter FRP III), the systo-diastolic diameter (echotracking technique) and the mean blood flow velocity and volume of the common carotid artery, the blood viscosity (rotational viscometer) and the finger arterial blood pressure (Finapress Ohmeda) were measured in 12 young volunteers (aged 25+/-2 years) and in 12 elderly hypertensives (aged 80+/-4 years) treated with short-acting calcium antagonists up to 24h before the study, both at baseline and after intravenous furosemide infusion (0.5mg/min), when the haematocrit had increased by at least two percentage points. After furosemide administration the mean arterial blood pressure decreased and blood viscosity and carotid systolic shear stress increased in both groups. However, common carotid artery diameter increased only in the young controls but not in the elderly hypertensives. These data show that an increase in carotid shear stress caused by haemoconcentration induces carotid vasodilatation only in young healthy subjects, and not in elderly hypertensives. This effect may be related to impaired endothelium function and/or arterial wall mechanics.

Effects of prolonged high-altitude exposure on peripheral adrenergic receptors in young healthy volunteers.

The regulation of adrenergic receptors during hypoxia is complex, and the results of published reports have not been consistent. In the present study blood cell adrenoceptor characteristics at sea level (SL) before and after prolonged exposure to high altitude (HA) were measured in seven trained young male lowlanders. Sympathoadrenal activity and clinical haemodynamic parameters were also evaluated before departure (SLB), after 1 week (HA1) and 4 weeks (HA4) at HA and 1 week after return to sea level (SLA). As compared to pre-departure sea level values, urinary norepinephrine excretion increased significantly during altitude exposure [SLB: 10.26 (3.04) microg x 3 h(-1); HA1: 23.2 (4.19) microg x 3 h(-1); HA4: 20.3 (8.68) microg x 3 h(-1)] and fell to pre-ascent values 1 week after return to sea level [SLA: 9 (2.91) microg x 3 h(-1)]. In contrast, mean urinary epinephrine levels did not increase over time at HA. Both systolic and diastolic blood pressures, as well as heart rate, were increased during HA exposure. The circadian blood pressure and heart rate rhythms were preserved during all phases of altitude exposure. Mean maximal binding (Bmax) of the alpha2-adrenoceptor antagonist [3H]rauwolscine to platelet membranes was significantly reduced (P < 0.001) after exposure to chronic hypoxia [SLB: 172.6 (48.5) fmol x mg(-1) protein versus SLA: 136.8 (56.1) fmol x mg(-1) protein] without change in the dissociation constant (K(D)). Neither the lymphomonocyte beta2-adrenoceptor Bmax [SLB: 38.5 (13.6) fmol x mg(-1) protein, versus SLA: 32.4 (12.1) fmol mg(-1) protein] nor the K(D) for [3H]dihydroalprenolol was affected by chronic hypoxia. Cyclic AMP (adenosine 3',5'-cyclic monophoshate) generation in lymphomonocytes by maximal isoproterenol stimulation was not modified after prolonged HA exposure. In conclusion, the down-regulation of alpha2-adrenoceptors appears to be an important component of the adrenergic system response to HA exposure.

Systemic and regional haemodynamic effects of aortofemoral angiography.

UNLABELLED: The aim was to investigate the regional and systemic haemodynamic consequences of bolus injection of fluids with different physical properties in the course of routine aortography. Iopamidol was compared with an equiosmolar solution of mannitol and with a 0.9 N saline solution. Continuous blood flow and Pulsatility Index (PI), as an index of regional vascular resistance, were measured by Doppler technique. Finger arterial pressure and heart rate were monitored at the time and for 3 min following each intraaortic bolus injections. The patients who underwent routine aortography were grouped according to the site of the flow measurements: common femoral artery, common carotid artery and brachial artery. Flow changes induced by the bolus infusion were evident for all the fluids but only at the femoral artery level. After an immediate (3 +/- 2 s) and brief (2 +/- 2 s) but marked reduction of flow and in-phase increase of PI following the bolus, further haemodynamic changes were observed only in the femoral artery, with a peak at 35 +/- 10 s and returning to baseline values after 70 +/- 15 s, in terms of both increased mean blood velocity and decreased PI. Saline and mannitol induced overall blood velocity alterations of 54% and 80%, respectively, and PI reductions of 44% and 57% compared with those induced by iopamidol. In the other vascular areas there was only a 17 +/- 2% increase of the physiological early diastolic backflow at the brachial artery level. Blood pressure decreased and heart rate increased in phase with the flow changes of the femoral artery. IN CONCLUSION: (1) a dramatic rheodynamic perturbation at the site of injection induces a vasodilating stimulus; (2) the haemodynamic response following injection results in marked vasodilation of only the tributary vascular bed; (3) flow steal may occur from other beds towards the lower limb vascular beds owing to vascular impedance imbalance; (4) a reduction of systemic arterial pressure is induced in phase with the regional vascular events and a reflex increase of the heart rate; and (5) the physical properties of the injected fluids influence the intensity of the perturbation, although the decisive triggering factor is the counterflowing bolus per se.

Inhibition of trophoblast adhesion to endothelial cells by the sera of women with recurrent spontaneous abortions.

PROBLEM: May anti-phospholipid or other autoantibodies interfere with trophoblast-endothelial cells interaction in women with unexplained pregnancy losses? METHODS OF STUDY: The sera of 72 women with recurrent spontaneous abortions (RSA) containing antibodies to endothelial cells (28), trophoblast (14), and cardiolipin (10) or lacking antibodies (25), and 26 controls were examined in an inhibition assay of trophoblast adhesion to endothelial cells using an ELISA based on the recognition of trophoblast by antibodies to cytokeratin. RESULTS: Adhesion of trophoblast to endothelial cells was time- and dose-dependent. Patients and control sera inhibited trophoblast adhesion with mean values of 37% and 7%, respectively. Inhibition above 2SD of the mean control value was still observed in 58% of the patients sera and 8% of the control sera. Sera containing antibodies to endothelial cells had higher inhibitory effect (38%) than those with antibodies to trophoblast (23%) and cardiolipin (28%) or lacking antibodies (26%). CONCLUSIONS: Antibodies and other undefined factors in the sera of women with RSA inhibit adhesion of trophoblast to endothelial cells.

Baroreceptor-heart rate reflex sensitivity enhancement after urinary bladder distention in essential hypertensives.

Our objective was to determine if urinary bladder distention modifies the sensitivity of the baroreceptor-heart rate reflex in hypertensive and control subjects. The baroreceptor-heart rate reflex sensitivity was measured in 15 male patients (mean age 37+/-8 years) with mild untreated hypertension (mean 163+/-8/ 95+/-12 mmHg) and 17 age- and sex-matched control subjects before and after urinary bladder distention. Bladder filling was performed infusing saline heated to 37 degrees C via a urinary catheter; the volume infused in each patient corresponded to that which caused the urge to void without reaching the pain threshold. The baroreceptor-heart rate reflex sensitivity was determined correlating the variations of the systolic pressure and of the peak blood flow velocity in the common carotid artery with the variations of the ECG RR' interval of the following heart beat, both during spontaneous and phenylephrine-induced fluctuations of the haemodynamic variables. After bladder distention the diastolic pressure of the hypertensive subjects increased significantly (95+/-12 vs. 100+/-12 mmHg: P < 0.02), whereas the heart rate decreased (RR= 873+/-70 vs. 926+/-80 ms; P < 0.005). These parameters were unchanged in the normotensive subjects (84+/-9 vs. 83+/-8 mmHg and 914+/-158 vs. 913+/-140 ms, respectively). The baroreceptor-heart rate reflex sensitivity, measured on the basis of spontaneous pressure and carotid blood flow velocity fluctuations in relationship to RR changes, decreased in the normotensive subjects after bladder distention (10.7+/-4.6 vs. 9.4+/-2.7 ms/mmHg; P < 0.05 and 423+/-99 vs. 356+/-102 ms/kHz; P < 0.01, respectively), whereas it increased in the hypertensive patients (6.9 +/- 3.6 vs. 8.3 +/- 2.8 ms/mmHg; P < 0.03, and 332 +/- 86 vs. 381+/-97 ms/kHz; P < 0.03 respectively). After bladder distention and phenylephrine administration the baroreceptor-heart rate reflex sensitivity, measured by the correlation between systolic pressure and RR interval, increased only in the hypertensive group (10.2+/-5.4 vs. 15.2+/-7.7 ms/mmHg; P < 0.005). In conclusion urinary bladder distention provokes in hypertensives but not normotensive controls a brisk parasympathetic response of the component of the baroreceptor-heart rate reflex which controls heart rate.

Complement-endothelial cell interactions: pathophysiological implications.

The function of the endothelial cells can be modulated by humoral factors present in the circulation and in the extravascular fluid, including proteins of the complement system. This review examines the multiple interactions between the complement system and the endothelial cells and their functional consequences on inflammation, coagulation and regulation of vascular tone. The implications of these interactions in the induction and progression of the vascular lesions occurring in atherosclerosis, ischemia/reperfusion and xenotransplantation and the possible therapeutic approaches in terms of complement regulation are also discussed.

Control of glomerular hyperfiltration and renal hypertrophy by an angiotensin converting enzyme inhibitor prevents the progression of renal damage in hypertensive diabetic rats.

OBJECTIVE: Glomerular hyperfiltration and renal hypertrophy are both considered important in the progression of diabetic nephropathy. The aim of this study was to compare the effects of an equivalent reduction in blood pressure produced by the angiotensin-converting enzyme (ACE) inhibitor spirapril (SPI) and an antihypertensive triple drug combination of hydralazine, reserpine and hydrochlorothiazide (HRH) on kidney function, proteinuria and renal structure in hypertensive diabetic rats. DESIGN AND METHODS: Four groups of animals were evaluated in short-term and long-term studies. In both studies one group served as a non-diabetic hypertensive control (H). The other three groups were rendered diabetic and were allocated to one of the following groups: the first diabetic group received no specific therapy (HD), the second diabetic group was treated with SPI (HD-SPI) and the third diabetic group was treated with HRH (HD-HRH). In each of the two studies the systolic blood pressure (SBP), 24 h urinary total protein, glomerular filtration rate (GFR), glomerular area, proximal tubular area and glomerular sclerosis were evaluated. RESULTS: The blood pressure reduction was equal in rats receiving either SPI or HRH. The GFR, proteinuria, glomerular area and tubular area were significantly increased in the HD group, both in the short-term and the long-term study. In the HD-SPI group the diabetic hyperfiltration and renal hypertrophy responses were prevented. In the HD-HRH group the GFR and proteinuria were slightly reduced in the later phases of diabetes, while the glomerular area and tubular area were not affected. Semiquantitative analysis of renal lesions showed that SPI was more effective than HRH in the prevention of the development of glomerulosclerosis. CONCLUSIONS: The results of this study suggest that the control of early adaptive hyperfiltration and renal hypertrophy by SPI may be relevant in the prevention of glomerulosclerosis.