Rupesh Raina

The early use of transurethral alprostadil after radical prostatectomy potentially facilitates an earlier return of erectile function and successful sexual activity.

To assess whether early introduction of the Medicated Urethral System for Erection (MUSETM, Vivus Inc., Mountain View, CA, USA) after radical prostatectomy (RP) results in a shorter recovery time for the return to functional erections and successful sexual activity.

Early combination therapy: intracavernosal injections and sildenafil following radical prostatectomy increases sexual activity and the return of natural erections.

Early pharmacological prophylaxis has been reported to increase the return of spontaneous erections following radical prostatectomy (RP). In this study, we evaluated the role of intracavernosal alprostadil (PGE1) combined with sildenafil in stimulating early recovery of spontaneous erections following RP. In this prospective study, we included 22 patients who underwent bilateral nerve-sparing RP after October 2004. Sildenafil dose of 50u2009mg/day was started at the time of hospital discharge. Of 22 patients, 18 started on PGE1–4u2009μg (1–8) and four started on low-dose Trimix (20u2009U) 2–3 times/week. These patients are followed up at regular intervals (3, 6, 9 and 12 months) with abridged version of the International Index for Erectile Function-5 questionnaire. Patient compliance, return of sexual activity and return of natural erection, adverse effects and reasons for discontinuation were recorded. Penile doppler studies were performed during followup visits to assess the vascular status. After a mean followup of 6 months (3–8 months), 11/22 (50%) patients had return of spontaneous partial erections. Of the 18 PGE1 users, six continued 4u2009μg PGE1, four increased the dose to 8u2009μg, six decreased the dose to 2u2009μg and two patients further reduced the dose to 1u2009μg. Of four low-dose Trimix users, three increased the dose to 30u2009U and one reduced the dose to 15u2009U. Of 22 patients, 21 were sexually active: 12/21 (57%) with the injections alone and 9/21 (42.9%) with combination therapy (injections (PGE1) and sildenafil). Penile doppler studies revealed arterial insufficiency in 77% (17/22) patients and venous insufficiency in one patient. Early intracavernosal injections following RP facilitated early sexual intercourse, patient satisfaction and potentially earlier return of natural erections. Early combination therapy with sildenafil allowed a lower dose of intracavernous injections, minimizing the penile discomfort.

Early penile rehabilitation following radical prostatectomy: Cleveland clinic experience

Erectile dysfunction is one of the most important quality of life issues following radical prostatectomy. The potency rates reported following nerve-sparing technique varies between 40 and 86%, and the time period required for complete recovery of erectile function varies from 6 to 24 months. The literature evidence suggests that lack of natural erections during this period of time produces cavernosal hypoxia. Prolonged periods of cavernosal hypoxia induce fibrosis, which later increases the incidence of venous leak. Recently, there is a growing interest among the physicians to interrupt these events by preventing cavernosal hypoxia during the period of neuropraxia. Initial studies using intracavernosal injection appears to be beneficial. In this article, we reviewed the pathophysiology of cavernosal hypoxia following radical prostatectomy with currently available evidence for the interventions to promote the nerve recovery and regeneration.

Finding the cause of acute kidney injury: which index of fractional excretion is better?

The fractional excretion of urea (FEU) is a useful index for differentiating the main categories of causes of acute kidney injury, ie, prerenal causes and intrinsic causes. It may be used in preference to the more widely used fractional excretion of sodium (FENa) in situations in which the validity of the latter is limited, such as in patients taking a diuretic. In patients on diuretics, fractional excretion of urea should be used in preference to fractional excretion of sodium.

Effect of amphotericin B lipid complex (ABLC) in very low birth weight infants

The aim of this retrospective, case–control study was to determine the effect of the amphotericin B lipid complex (ABLC) on serum creatinine (SCr), blood urea nitrogen (BUN), sodium (Na), and potassium (K) in very low birth weight (VLBW) infants. Medical records of all VLBW infants who were admitted to our Neonatal Intensive Care Unit between May 1998 and May 2006 and had received ABLC for at least 2xa0weeks were reviewed for patient demographics, use of medications (ABLC, diuretics, xanthines, indomethacin, vancomycin, gentamicin, pressors, and inotropes), fluid intake, urinary output, and serum electrolytes. Thirty-five patients who received ABLC were identified and matched by gestational age (GA) to 35 patients who served as controls. Infants who received ABLC had an average GA of 25.7u2009±u20092.1xa0weeks and a birth weight of 764u2009±u2009196 g. Between day 1 and 14 of ABLC treatment, the BUN decreased from 17.5u2009±u200911.5 to 10.5u2009±u20096.8xa0mg/dl (pu2009=u20090.01), the SCr varied between 0.78u2009±u20090.32 and 0.69u2009±u20090.32xa0mg/dl, Na varied between 136.6u2009±u20095.8 and 137.8u2009±u20093.6xa0mEq/l, and K varied between 4.8u2009±u20090.9 and 4.9u2009±u20090.6xa0mEq/l, respectively. Based on these results, we conclude that treatment with ABLC for 2xa0weeks did not increase BUN or SCr, nor decrease Na or K in VLBW infants.

Outcome of extremely low birth weight infants with a history of neonatal acute kidney injury

ObjectiveTo study the outcome of extremely low birth weight (ELBW) infants with a history of acute kidney injury (AKI).MethodIn a retrospective, case control study, medical records of all ELBW infants admitted to the neonatal intensive care unit (NICU) between Jan 2002 and Dec 2011 were reviewed. Medical records were reviewed for infants’ demographics, blood pressure (BP) at NICU discharge and at ≥3xa0years, and estimated glomerular filtration rate (eGFR) at ≥2xa0years.ResultsDuring the study period, 222 patients met the inclusion criteria, of whom 10% (23 out of 222) had AKI stage 2 and 3, 39% (87 out of 222) had AKI stage 1, and the rest did not have AKI. At NICU discharge, there was a difference in diastolic BP (DBP) among infants who had AKI stages 2 and 3, those who had stage 1, and those who did not have AKI (53u2009±u200912 vs 46u2009±u20099 vs 46u2009±u200911xa0mmHg respectively; pu2009=u20090.007), and 11% (23 out of 209) had hypertension (HTN). Although there was a significant correlation between the rise in SCr and DBP at NICU discharge in infants with AKI (Ru2009=u20090.304; pu2009=u20090.004), there was no difference in HTN between infants with and those without AKI. At ≥2xa0years of age, 4% (5 out of 120) across all groups had an eGFRu2009<u200990xa0ml/min/1.73m2 or chronic kidney disease (CKD). At ≥3xa0years of age, 5% (11 out of 222) had HTN.ConclusionAt NICU discharge, infants with AKI stages 2 and 3 have a higher DBP than infants with stage 1 AKI and those who did not have AKI. However, there is no difference in the rate of HTN between the two groups. At ≥2xa0years ELBW infants are at risk for CKD independently of whether or not they develop neonatal AKI.

Relationship of urinary endothelin-1 with estimated glomerular filtration rate in autosomal dominant polycystic kidney disease: a pilot cross-sectional analysis

BackgroundThe pathogenesis of progressive renal insufficiency in autosomal dominant polycystic kidney disease (ADPKD) is unclear. Evidence from experimental models of ADPKD suggests that elevated endothelin-1 (ET-1) drives cyst growth, renal fibrosis and loss of renal function, but whether ET-1 is elevated in humans with ADPKD is uncertain.MethodsIn a cross-sectional study of ADPKD we measured urinary ET-1, a surrogate for ET-1 in kidney cortex, in spot collections corrected for creatinine. The volume of each kidney was measured using MRI-based stereology. The relationship of urine ET-1 with MDRD eGFR and kidney volume was modeled by multiple linear regression with adjustment for clinical covariates.ResultsPatients with ADPKD were ages 18 to 53 with eGFRs (median, interquartile range) of 63.2 (43.5–80.2) ml/min/1.73xa0m2 and albumin/creatinine ratios (ACR) of 115.0 (7.5–58.5) μg/mg. Urine ET-1 was inversely associated with eGFR (ru2009=u2009−0.480, Pu2009<u20090.05) and positively (ru2009=u20090.407, Pu2009=u20090.066) with ACR independent of age and female sex (Pu2009<u20090.01). ET-1 appeared to be positively associated with total kidney volume (ru2009=u20090.426, Pu2009=u20090.100), with a test for trend across urine ET-1 quartiles yielding zu2009=u20091.83, Pu2009=u20090.068. ET-1 strongly correlated with NAGase (ru2009=u20090. 687, Pu2009=u20090.001), a marker of tubular damage and a surrogate marker of renal disease progression in ADPKD. Of note, ET-1 levels in urine were not correlated with hypertension.ConclusionsIn a translational study of patients with ADPKD, urinary ET-1 was inversely associated with eGFR and positively correlated with total kidney volume. Taken together with results from experimental models, these findings suggest that the role of ET-1 in ADPKD warrants further investigation.

Treatment of erectile dysfunction: update.

Erectile dysfunction (ED) is the inability to achieve and maintain an erection. Erectile function is dependent upon complex interactions of neural and vascular pathways. A major neurotransmitter that facilitates erectile function is nitric oxide. Treatment of ED has expanded to include effective oral agents. Previous ED treatments have consisted of intracavernosal injection, transurethral dilators, and vascular constriction devices. Clinical management of ED will be presented with some discussion on the prostatectomy client.

Muscle Weakness and Pain With Profound Hypophosphatemia Mystery Revealed

A 14-year-old male with a history of septo-optic dysplasia, panhypopituitarism, and epilepsy presented for inpatient evaluation after laboratory studies for his worsening muscle weakness and muscle pain found new onset normoglycemic glucosuria and proteinuria (urinary protein/creatinine ratio of 2.9 with minimal albumin fraction). The year prior to admission, he became gradually unable to ambulate and was wheelchair bound. Orthopedic and neurologic evaluations for his progressive weakness and difficulty with ambulation were unrevealing to date. Laboratory evaluation on admission showed profound hypophosphatemia (0.6 mg/dL), a nonanion gap metabolic acidosis, and normal kidney function (creatinine = 0.4 mg/dL). In addition, he had hyperuricosuria, (fractional excretion of urate 64%; normal, <15%), increased fractional excretion of sodium (1.5%), reduced tubular phosphate reabsorption (78%), and mild hypercalciuria.