[The hemodialysed patient and his/her family caregiver. Comparison of perceptions of the chronic illness]. / Il paziente emodializzato e il caregiver familiare. Percezioni a confronto sulla malattia cronica.

BACKGROUND: According to health psychology, the family caregiver (fc), i.e. the person who takes care of a hemodialysed patient, plays a pivotal role in coping with dialysis. This study explored and compared the lifestyle and the main needs of a cohort of hemodialysis patients, with reduced personal autonomy, to their fc, evaluating some psychological functional parameters, such as the perception of familial and social support, the psychological quality of life, the disability due to chronic illness, and the communication style. METHODS: An anonymous multiple versions questionnaire, administered according to the caregiver's family relationship, was given for self assessment to 54 couples of patients and related fc (spouse, son/daughter and brother/sister), mean age 66 and 60, respectively; mean dialytic patients' age: 8 years and 6 months. The questionnaire consisted of three different sections, demographics, renal disease and psychological evaluation, with 4 standard scales (Social Support Satisfaction, Marital Communication, Psychological General Well-Being Index and Evaluation of Needs). A multivariate variance analysis (MANOVA) was subsequently performed. RESULTS: Women have a higher perception of their lifestyle change after dialysis, and, in general, patients communicate more easily with their fc than vice versa. Communication problems are more common in patients with a recent diagnosis. Patients and fc mostly need a better dialogue with their nephrologists and urge some psychological help. CONCLUSIONS: The quality of the relationship between physicians, patients and their families is a key element in the process of healing.

Medical prevention and treatment of urinary stones.

Despite revolutionary developments in minimally invasive methods for the removal of stones in the last 15 years, the medical prevention of urinary stones remains very rewarding, due to the continual increase in the prevalence of nephrolithiasis in western countries, the high recurrence rate of the disease, its complications, discomfort and the costs of lithotripsy. Medical prevention is highly effective (50-95% efficacy in different series) and cost-convenient; its basic elements are appropriate metabolic evaluation, adequate hydration, "common sense" diet, and, in selected cases, drugs of proven efficacy. Clinical-metabolic evaluation should aim at the recognition of specific types of nephrolithiasis, and sort out secondary and/or remediable cases, define urinary risk factors, assess patients' compliance and the side effects of any therapy during follow-up. Hydration has proved effective in clinical trials and population-based observational studies; "fluids" may consist of water (any kind), coffee (caffeinated or decaffeinated), tea, beer and wine; grapefruit juice appears to have an unexplained ill effect. Despite the lack of clinical demonstration that dietary manipulations reduce the recurrences of stones, biochemical and epidemiological data suggest that high sodium, animal protein and sucrose intake increase the risk. Undue reductions in Ca intake also appear to be detrimental both for stone recurrences and bone mineralisation: "adequate" Ca intake (800-1000 mg/day) should be encouraged, but only in food since supplemental Ca, as drugs, appears to increase the risk of stones. Effective drugs are available for cystine, uric acid, infected stones and several secondary causes of Ca nephrolithiasis; in "idiopathic" Ca nephrolithiasis, thiazides, allopurinol, K and K-Mg citrate and possibly neutral K phosphate have been shown to be effective, at least in specific metabolic contexts.

Abnormal reabsorption of Na+/CI- by the thiazide-inhibitable transporter of the distal convoluted tubule in Gitelman's syndrome.

Eleven patients with Gitelman's syndrome and 23 controls underwent acute administration of the thiazide diuretic hydrochlorothiazide and/or the loop diuretic furosemide (FUR) in order to indirectly evaluate the activity of the two electroneutral Na+/Cl(-)-reabsorptive systems of the distal nephron, namely the thiazide-sensitive Na+-Cl- symporter of the distal convoluted tubule and the FUR-sensitive Na+-K+-2Cl- symporter of the loop of Henle. The patients were characterized by hypokalemia, mild metabolic alkalosis, hypomagnesemia, hypocalciuria, and reduced free water generation during maximally diluted diuresis which indicated reduced distal nephron NaCl reabsorption. The plasma Na and Cl levels were similar in patients and controls. Hydrochlorothiazide induced a significantly lower increase of urinary Na and Cl excretions in 6 patients with Gitelman's syndrome than in 6 controls, indicating reduced NaCl reabsorption by the thiazide-sensitive Na+/Cl- symporter of the distal convoluted tubule in Gitelman's syndrome. FUR induced a slightly higher increase of urinary Na and Cl excretions in 11 patients with Gitelman's syndrome than in 17 controls, in keeping with reduced NaCl reabsorption in tubular sites past the loop of Henle during FUR effect or increased NaCl reabsorption in the loop itself (as a compensatory mechanism for NaCl-reabsorptive defect in the distal convoluted tubule) or both. Our results confirm that the functional activity of the renal thiazide-sensitive Na+-Cl- cotransporter (but not of the FUR-sensitive carrier) is deficient in patients with Gitelman's syndrome, in keeping with the recently described genetic link between the syndrome and a wide variety of nonconservative mutations of the gene encoding the protein; it is suggested that dynamic studies with diuretic administration may be of diagnostic help in this condition.

Correction of hypokalemia with antialdosterone therapy in Gitelman's syndrome.

Six adult patients (4 females and 2 males, age range 26-57 years) with Gitelman's syndrome (GS) were treated with spironolactone 200-300 mg/day (n = 5) and/or amiloride 10-30 mg/day (n = 3) for 1-18 months. The patients had hypokalemia, hyperreninemia, chloride-resistant metabolic alkalosis, renal hypomagnesemia (n = 5), and hypocalciuria (n = 5). Free water clearance studies during maximal water diuresis and furosemide administration were suggestive of a solute reabsorptive defect beyond the loop of Henle. Antialdosterone therapy induced a significant increase of PK (from 2.6 +/- 0.4 to 3.4 +/- 0.4 mM; p < 0.0001) and a decrease of CK (from 21.4 +/- 13.2 to 10.6 +/- 4.8 ml/min, p < 0.02) and FEK (from 21.0 +/- 13.6 to 13.4 +/- 5.7%; p < 0.03); PMg increased from 1.38 +/- 0.38 to 1.64 +/- 0.21 mg/dl (p < 0.03) with a parallel fall of CMg (from 5.5 +/- 2.3 to 2.9 +/- 1.5 ml/min; p < 0.02) and FEMg (from 5.7 +/- 2.6 to 2.9 +/- 0.6%; p < 0.05); arterial blood pH and HCO3- did not change (P = plasma, C = clearance, FE = fractional excretion). The creatinine clearance fell (from 90.5 +/- 16.8 to 65.8 +/- 20.9 ml/min; p < 0.05), and Prenin rose (from 16.6 +/- 8.9 to 35.3 +/- 25.3 ng/ml/h; p < 0.02, as did Paldo (from 26.1 +/- 12.3 to 109 +/- 82.6 ng/dl; p < 0.01), indicating extracellular fluid volume contraction; however no significant clinical symptoms of hypovolemia ensued.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac arrhythmias and electrolyte changes during haemodialysis.

Cardiac arrhythmias are a frequent event in chronic haemodialysis patients, and their pathogenesis is still poorly understood. We evaluated plasma K+ (PK), intraerythrocytic K+ (EK) and acid-base changes during haemodialysis in six patients with frequent arrhythmias (A-pts), and in six (used as controls) nonarrhythmic dialysis patients (C-pts). PK decreased significantly (P less than 0.01) during haemodialysis in both groups: A-pts (pre HD: 4.81 +/- 0.52 mM; 1st hour: 3.66 +/- 0.44; end HD: 3.17 +/- 0.38) and C-pts (4.75 +/- 0.80; 3.71 +/- 0.32 and 3.18 +/- 0.18 respectively) without any significant difference at any time between the two groups. Predialysis arterial pH and HCO3 were similar in A-pts (7.33 +/- 0.07 and 22.1 +/- 4.5 mM) and C-pts (7.29 +/- 0.04 and 19.7 +/- 2.6 mM) but an apparently better correction of acidosis within the treatment was seen in A-pts (arterial pH 1st hour: 7.38 +/- 0.07; end HD: 7.39 +/- 0.07) than C-pts (1st hour: 7.31 +/- 0.02, P less than 0.05 versus A-pts; end HD: 7.33 +/- 0.03, P less than 0.05 versus A-pts). EK was significantly (P less than 0.01) greater at all times in C-pts (pre HD: 90.6 +/- 15.7 mmol/l RBC; 1st hour: 93.3 +/- 11.7; end HD 96.6 +/- 10.7) than A-pts (72.1 +/- 9.0; 77.2 +/- 3.7 and 79.3 +/- 8.4, respectively). We conclude that haemodialysis patients with arrhythmias have a decreased intraerythrocytic K content in comparison with other patients despite similar PK values; this finding might constitute a predisposing factor for arrhythmias.

Pseudo-Bartter's syndrome from surreptitious diuretic intake: differential diagnosis with true Bartter's syndrome.

Five patients with pseudo-Bartter's syndrome from surreptitious diuretic abuse were compared with six patients with true Bartter's syndrome, diagnosed as a normotensive, hyperreninaemic, hypokalaemic metabolic alkalosis with normal urine chloride excretion, low CH2O/(CH2O+CCl) ratio during maximal water diuresis and negative urine screen for diuretics. The latter was positive for frusemide in four and for hydrochlorothiazide in the remaining pseudo-Bartter's patients. The two groups of patients did not differ as for plasma Na+, Cl-, K+, HCO3-, renin, and aldosterone, while uric acid and Mg2+ were greater in pseudo-Bartter's patients. Daily and fasting urine Na+, Cl- and K+ excretion were less in pseudo-Bartter's patients; however, there was substantial overlap of values between the two groups. Fractional distal solute reabsorption during maximal water diuresis was low in the six patients with Bartter's syndrome and in two pseudo-Bartter's patients; thus, this parameter could not be taken as a specific diagnostic marker of Bartter's syndrome. Frusemide administration, 40 mg i.v., induced a brisk increase of urine flow (11.7-21.8 ml/min), UOsm (148-186 mOsm/kg H2O) and FENa (14.6-24%) in Bartter's syndrome, but not pseudo-Bartter's patients; in all pseudo-Bartter's patients frusemide-induced changes of UOsm (13-97) and FENa (-0.5 to 10.2) were markedly less than in Bartter's syndrome patients. Frusemide resistance in pseudo-Bartter's patients was most probably related to diuretic-induced ECF volume contraction and increased proximal tubule solute reabsorption; in fact fractional lithium clearance (FELi, a marker of post-proximal solute delivery) was low in pseudo-Bartter's, but not in Bartter's syndrome patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acute administration of acetazolamide and frusemide on lithium clearance in humans.

To investigate the mechanism(s) of acute frusemide-induced increases in FELi, the effects of frusemide and acetazolamide, the carbonic anhydrase inhibiting agent, were evaluated in 19 healthy subjects either before or after pretreatment with acetazolamide or frusemide (11 subjects and eight subjects respectively). Acetazolamide pretreatment did not modify frusemide-induced increases in FELi (delta FLi 12.8 +/- 4.1% compared to 14.6 +/- 7.3%, P = NS); similarly, frusemide pretreatment did not modify acetazolamide-induced increases in FELi (delta FLi: 11.3 +/- 5.9% compared to 9.8 +/- 3.8%, P = NS). Acetazolamide-induced changes of FELi were correlated significantly with acetazolamide-induced increases of FEHCO3 (r = 0.61, P less than 0.05), FENa (r = 0.46, P less than 0.05) but not of FECl (r = 0.25, P = NS). On the other hand, frusemide-induced changes of FELi were correlated significantly with frusemide-induced increases of FENa (r = 0.62, P less than 0.005), FEC1 (r = 0.52, P less than 0.025) but not of FEHCO3 (r = 0.3, P = NS). Thus, frusemide effects on tubular lithium reabsorption are not related to carbonic anhydrase inhibition; furthermore, it appears that frusemide and acetazolamide affect lithium reabsorption by different and independent mechanism(s), possibly acting at different nephron site(s).

The changes in plasma diffusible levels and renal tubular handling of magnesium during pregnancy: a longitudinal study.

Magnesium fasting plasma levels (total, PMg, and ultrafiltrable, PMgUF), daily urinary excretion and tubular reabsorption in the fasting state were measured in 14 healthy women along an uncomplicated gestation and compared with the values observed 3-6 months after delivery (C). PMg and PMgUF progressively fell during gestation (from 1.96 +/- 0.14 and 1.38 +/- 0.09 mg/dl in C, respectively, to 1.67 +/- 0.13 (P less than 0.0005) and 1.2 +/- 0.09 (P less than 0.0005) after 17-26 weeks of gestation and to 1.66 +/- 0.10 (P less than 0.0005) and 1.17 +/- 0.08 (P less than 0.0005) after 27 weeks to term). The decrease in PMg and PMgUF was further apparent in an additional group of 46 pregnant women in comparison with 20 sex-matched non-pregnant controls. Urinary Mg excretion remained unchanged throughout gestation, as did glomerular filtered load of PMgUF and tubular Mg reabsorption in the fasting state, due to the increase in GFR. Moreover, urinary Mg excretion per unit GFR (MgE, mg/dlGFR) and fractional excretion of MgUF filtered load (FEMgUF, %) fell (from 41 +/- 25 and 3.0 +/- 0.9 in C, respectively, to 26 +/- 12 (P less than 0.01) and 2.2 +/- 1.0 (P less than 0.05] in the last period, indicating that a greater fraction of filtered Mg was being reabsorbed by renal tubules. There was a significant inverse correlation between PMgUF and GFR in all the periods studied (r = 0.39, P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)