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The Experience Heart and kidney diseases are closely related and the term “cardio renal syndrome” is adopted worldwide to underline that linkage. Richard Bright recognized that “hypertrophy of the heart seems in some degree to have kept pace with the advance of the disease in the kidneys” and, after him, George Johnson, William Gull, Henry Sutton, Franz Volhard, Theodor Fahr, and Henry Goldblatt confirmed Bright’s hypothesis. In 1956, Gabriele Monasterio et al, the Pisa School of Medicine introduced the term “Renal Cardiopathy”. Further meetings, such as Strasburg, Giessen and especially Assisi Cardionephrology meeting, have emphasized this relationship, after 25 years of experience largely thanks to Professor Timio. On the other hand, the Advanced Dialysis Quality Initiative, led by Prof. Claudio Ronco from Vicenza (Italy), has contributed greatly to the definition and classification of the “Cardio-Renal Syndromes”.

To the Editor Nutcracker syndrome commonly refers to left renal vein compression between aorta and superior mesenteric artery, resulting in increased venous pressure, kidney congestion and proteinuria. Posterior nutcracker syndrome is a rare variant, linked to retro-aortic position of the last tract of the left renal vein which remains compressed between aorta and spinal column. We report an unusual case of posterior nutcracker syndrome in a 22-year-old man with congenital solitary left kidney who was admitted to our department because of proteinuria of 700 mg/24 h and microhematuria. Upon admission, blood pressure was 120/70 mmHg. Mild pitting edema was present in his lower limbs. Laboratory workup showed a normal renal function with a creatinine of 1.1 mg/dl. Urinalysis revealed the presence of rare hyaline and granular casts and isomorphic erythrocytes. No previous episodes of left flank pain were reported. Ultrasonography was performed showing the absence of the right kidney, compensatory hypertrophy of the left organ and dilation of the left renal vein. After a few centimeters from the hilum, the left renal vein presented an abnormal course, addressed in cranio-caudal direction until merging into inferior vena cava just below common iliac arteries (Fig. 1a). Proximal venous dilation was also noted (antero-posterior diameter 13.8 mm in the hilar area, 1.6 mm in the narrow portion, ratio 8.6). Doppler peak velocities were 25 cm/s in the hilar area and 111 cm/s in the narrow portion (ratio 4.4). An abdomen contrast-enhanced computed tomography was then carried out, confirming the anomalous course of the vein. Compression of the vein was evident between left common iliac artery and a lumbar vertebral body (Fig. 1b, c). In order to confirm the diagnosis, a right femoral vein approach was performed, and the left renal vein was visualized in a contrast-enhanced phlebography (Fig. 1d). It was dilated, with a pressure gradient of 8 mmHg versus inferior vena cava. Endovascular stenting was then carried out and a self-expandable 14–40 mm stent made of nitinole was inserted where the vein narrowed. Post-procedural phlebography documented normal flow through the vessel, with no significant pressure gradient between the left renal vein and inferior vena cava. 24-h proteinuria promptly fell below 300 mg/day. Posterior nutcracker syndrome is characterized by the abnormal retro-aortic position of the left renal vein and its subsequent compression between aorta and spinal column [1–3]. Similar to the ‘‘anterior nutcracker phenomenon’’, this syndrome usually leads to renal venous hypertension and it should be considered among the causes of recurrent left flank pain, proteinuria and hematuria. A. Granata (&) A. Clementi Nephrology and Dialysis Unit, San Giovanni Di Dio Hospital, Agrigento, Italy e-mail: antonio.granata4@tin.it

Introduction. Hydatid disease is a cyclozoonotic parasitic infestation caused by the cestodeEchinococcus granulosus. The cysts mainly arise in the liver (50 to 70%) or lung (20 to 30%), but any other organ can be involved, in abdominal and pelvic locations, as well as in other less common sites, which may make both diagnosis and treatment more complex. Isolated renal involvement is extremely rare.Case Presentation. We report a rare case of isolated renal hydatid disease in a 71-year-old man with a history of vague abdominal pain, anemia, fever, and microhematuria. Ultrasonographic examination revealed a complex cyst in the right kidney, including multiple smaller cysts with internal echoes. A magnetic resonance scan of the abdomen confirmed the findings, and hydatid cyst disease was diagnosed. Right nephrectomy was performed, and microscopic examination confirmed the diagnosis of hydatid cyst. Albendazole, 10 mg/kg per day, was given for 4 weeks (2 weeks preoperatively and 2 weeks postoperatively).Conclusion. Isolated primary hydatidosis of the kidney should always be considered in the differential diagnosis of any cystic renal mass, even in the absence of accompanying involvement of liver or other visceral organs.

Background: Healthy subjects and patients after successful kidney transplantation show a circadian rhythm for glomerular filtration rate and for the glomerular transport of macromolecules. We aimed to evaluate by bioelectrical impedance analysis (BIA) whether body hydration status also follows a circadian rhythm in patients with impaired renal function. Methods: The study was conducted on 28 subjects divided into 3 groups: 8 healthy volunteers, 8 patients affected by chronic kidney disease and 12 end-stage renal disease (ESRD) patients on hemodialysis. During 24 h, 9 BIA measurements were taken in every subject every 180 min. Results: BIA findings demonstrate that normal subjects have a circadian rhythm in hydration status that reaches maximum body water content at night, between 21.00 and 23.00 h. In patients with chronic kidney disease, this rhythm, with maximum at night, is maintained. The rhythm is also present in ESRD patients, if the residual diuresis is at least 500 ml/day, while there is no rhythm when residual diuresis is Conclusions: In normal subjects, body hydration status shows a circadian rhythm, which is weakened or lost in oligoanuric patients on dialysis, but partially maintained in subjects with preterminal uremia and in hemodialyzed patients with residual diuresis >500 ml/day.

Patients undergoing renal graft failure and returning to dialysis are often regarded to like facing for the first time a substitutive treatment, without considering the technical complications, the economical impact, and the psychological implications. This review attempt, to give answers to various questions, concerning the management of vascular access, the immunosuppressive therapy, the transplantectomy, the emotional and neuropsychic aspects, and the quality of life of graft-failed patients.

Vasopressin (AVP), an antidiuretic hormone, is known to induce hypervolemia and to regulate the renal expression of aquaporin-2 (AQP2) water channels, but it is not yet known whether the latter are involved in the pathogenesis of essential hypertension. The aim of the present study was therefore to make a comparative study of blood pressure (BP), urinary volume (UV), urinary osmolarity (uOsm), urinary AQP2 (uAQP2), and plasma AVP levels (PAVP) in male spontaneously hypertensive rats (SHR; n = 30) at 3, 7, and 12 weeks of age and in male Wistar-Kyoto rats (WKY, n = 30), also after the subcutaneous administration of OPC-31260 (OPC), a human AVP V(2) receptor antagonist. At 3 weeks, SHR had markedly higher uOsm and lower UV levels than WKY. At 7 weeks, SHR were hypertensive, showing increased uAQP2, PAVP, and uOsm levels and a decreased UV. At 12 weeks, no significant changes were observed in this condition. At 7 and 12 weeks of age, OPC-treated WKY rats showed significant reduction in BP and uOsm and increase in UV with respect to untreated animals. From 3 weeks of age, OPC-treated SHR presented significantly lower BP levels, higher UV levels, and lower uOsm than untreated animals. In treated WKY and SHR, uAQP2 levels were lower than in untreated animals. The PAVP appeared to be higher in OPC-treated rats from both strains. These findings suggest that AVP and the AQP2 are involved in the pathogenesis of hypertension in SHR.

SUMMARY: Background and Aim: Our aim was to evaluate QTc interval and QTc dispersion in 27 end-stage renal disease (ESRD) patients undergoing Acetate Free Biofiltration (AFB) in order to ascertain any correlations between the electrrocardiographic (ECG) parameters, serum Na+, K+, Ca++, Mg++ and intraerythrocytic Mg++ (Mg++e) concentrations. All measures were made at t0 (session beginning), t1 (first hour), t2 (second hour), t3 (third hour), and t4 (session end). Results: Blood pressure, heart rate, bodyweight and total ultrafiltration in the three dialysis sessions were constant. A significant progressive increase occurred in serum Ca++ during the sessions, while there was a significant diminution in serum K+. The pattern for Mg++ concentrations in serum and erythrocytes differed: in serum it decreased, whereas Mg++e increased. At t4, the QTc interval was reduced to a significant extent with respect to the baseline value. QTc dispersion significantly increased at t1 without there being significant variations at other times with respect to t0. At t2, t3 and t4, values promptly returned to baseline levels. QTc had a negative correlation with serum Ca++ levels at t4. In contrast, an inverse correlation was found between QTc dispersion and serum K+ at t1. No other correlations could be found between any other electrolytes, QTc interval or QTc dispersion. Conclusion: In conclusion, the decrease observed in the QTc interval at the end of an AFB session was inversely related to serum Ca++ concentrations. Moreover, an increase in QTc dispersion occurred during the first hour of the session, and was negatively correlated with serum K+.

Hemodialysis influences the transport of water through the erythrocytic membrane, and induces morphologic and functional modifications. Recently water channels, called aquaporins (AQP), have been identified on the membrane of red blood cells. The aim of the present study was, therefore, to evaluate any relationships between volumetric changes in erythrocytes (MCV), plasma osmolarity and membrane expression of AQP1 in 22 uremic patients during a hemodialysis session, and compare value with those in a control group of 22 healthy volunteers. Membranal AQP1 expression was evaluated using three methods: indirect immunofluorescence under confocal microscopy, immunoenzymatic method after membrane extraction, and immunoblotting. In uremic subjects, at baseline membrane AQP1 expression was significantly lower, whereas plasma osmolality was higher than in controls. At 1 and 2 h of replacement therapy, a progressive increase was observed in erythrocytic AQP1, values similar to those in controls being attained after 3.5 h. During the session osmolality values reduced progressively, becoming significantly lower than basal values. The mean erythrocytic corpuscular volume in patients with ESRD was significantly lower than in cntrols at baseline. This value increased during hemodialysis, attaining statistical significance with respect to the basal value at 3.5 h of dialysis. Close correlations were found between plasma osmolality and AQP1 values (r = –0.930; p < 0.05), and also between MCV and plasma osmolality trend (r = –0.909; p < 0.05). There was a linear correlation (r = 0.63, p < 0.05) between plasma AVP concentrations and plasma osmolality. The variations found in plasma osmolarity during hemodialysis, may induce AQP1 expression on the membrane of intact red blood cells.

Many previous studies have shown that aquaporin-2 (AQP2), the vasopressin-regulated water channel, is excreted in the urine and that the excretion increases in response to vasopressin. Moreover, recently a close correlation between AQP2 excretion in urine and kidney AQP2 expression has been demonstrated, showing that urinary excretion of AQP2 is a reliable indicator for AQP-2 function. As head-out water immersion causes an expansion in the central vascular volume equal to that induced by 2 liters of saline, without modifying plasma composition, we used immersion in water to evaluate if the response to acute expansion of the central vascular volume could involve vasporessin (AVP) and AQP2. In healthy subjects, concentrations of plasma atrial natriuretic factor (ANF) and AVP, and urinary AQP2 were measured during a 2-hour immersion period. In all subjects, immersion caused a prompt and marked increase in immunoreactive ANF (23.0 ± 2.12 pg/ml at second hour vs. 2.17 ± 0.42 pg/ml at baseline) and in urinary excretion of AQP2 (23.9 ± 2.69 pmol/mg creatinine at second hour vs. 4.42 ± 0.14 pmol/mg creatinine at baseline), while a significant decrease was found in plasma AVP. Recovery was associated with a prompt return to pre-study levels. These findings demonstrate that heat-out water immersion stimulates urinary excretion of AQP2 in absence of an increase in plasma AVP.