فهرست مطالب

Kidney Diseases - Volume:3 Issue: 2, Apr 2009

Iranian Journal of Kidney Diseases
Volume:3 Issue: 2, Apr 2009

  • تاریخ انتشار: 1388/02/25
  • تعداد عناوین: 13
|
  • Himanshu Sekhar Mahapatra, Robert Lalmalsawma, Narendra Pal Singh, Mahender Kumar, Suresh Chandra Tiwari Pages 61-70
    Very often, physicians confront with patients who have concomitant heart and kidney failure. The coexistence of kidney and heart failure carries an extremely bad prognosis. The exact cause of deterioration of kidney function and the mechanism underlying this interaction are complex, multifactorial in nature, and still not completely understood. Both the heart and the kidney act in tandem to regulate blood pressure, vascular tone, diuresis, natriuresis, etc. An extension to the Guytonian model of volume and blood pressure control is proposed called cardiorenal connection. Regulating actions of Guyton’s model were coupled to their extended actions on structure and function of the heart and the kidney changes in the rennin-angiotensin-aldosterone system, the imbalance between nitric oxide and reactive oxygen species, the sympathetic nervous system, and inflammation are the cardiorenal connectors to develop cardiorenal syndrome. Imbalance in this closed complex will often lead to deterioration of both cardiac and kidney function. The World Congress of Nephrology emphasized vast interrelated derangements that can occur in cardiorenal syndrome and proposed that the recent definition of cardiorenal syndrome be modified into categories whose labels reflect the likely primary and secondary pathology and time frame. For management, drugs that impair kidney function are undesirable, particularly in a population with already compromised or at risk of kidney function. In severe volume-loaded patients who are refractory to diuretics, management of cardiorenal dysfunction is challenging. In the absence of definitive clinical trials, treatment decision must be based on a combination of patient’s condition and understanding of individual treatment options
  • Farahnak Assadi Pages 71-79
    Primary hyperparathyroidism and malignancy are responsible for greater than 90% of all cases of hypercalcemia. Compared with the hypercalcemia of malignancy, hyperparathyroidism tends to be associated with lower serum calcium levels (< 12 mg/dL) and a longer duration of hypercalcemia (more than 6 months). The hypercalcemic symptoms are usually fewer and subtle. Hyperparathyroidism tends to cause kidney calculi, hyperchloremic metabolic acidosis, and the characteristics of metabolic bone disease osteitis fibrosa cystica, but no anemia. In contrast, hypercalcemia of malignancy is typically rapid in onset, with higher serum calcium levels, and more severe symptoms. Patients so affected show marked anemia, but they never have kidney calculi or metabolic acidosis. Parathyroid hormone assay is the most useful test for differentiating hyperparathyroidism from malignancy and other causes of hypercalcemia. In hyperparathyroidism, serum parathyroid hormone levels will be elevated. In other cases, the high serum calcium concentration usually results in suppression of parathyroid hormone. Treatment of hypercalcemia should be started with hydration. Loop diuretics may be required in individuals with renal insufficiency or heart failure to prevent fluid overload. Calcitonin is administered for the immediate short-term management of severe symptomatic hypercalcemia. For long-term control of severe or symptomatic hypercalcemia, the addition of biphosphonate is typically required. Among intravenous bisphosphonates, zoledronic acid or pamidronate are the agents of choice. Glucocorticoids are effective in hypercalcemia due to lymphoma or granulomatous diseases. Dialysis is generally reserved for those with severe hypercalcemia complicated with kidney failure.
  • Yagnik Bhalodia, Nilesh Kanzariya, Rameshvar Patel, Natavarlal Patel, Jitendra Vaghasiya, Nurudin Jivani, Hitesh Raval Pages 80-85
    Introduction. Evidence suggests that reactive oxygen species play a role in the pathophysiology of renal ischemia/reperfusion (I/R) injury. This study was designed to investigate the renoprotective activity of methanolic fruit extract of Benincasa cerifera in I/R-induced kidney failure in rats. Materials and Methods. Renal pedicles of 12 rats were occluded for 60 minutes followed by 24 hours of reperfusion. Six days prior to induction of I/R, 6 of the rats received Benincasa cerifera, 500 mg/kg, orally. Serum creatinine, urea, and uric acid levels were measured after the operation. At the end of reperfusion period, the rats were sacrificed. Superoxide dismutage, catalase, reduced glutathione, and renal malondialdehyde content were determined in the renal tissues. Results were compared with a group of rats with sham operation.Results. Renal I/R caused significant impairment of kidney function. Six-day administration of Benincasa cerifera, however, minimized this effect. Rats with renal I/R only showed significantly decreased activity of superoxide dismutage, catalase, and reduced glutathione compared with the sham-operated rats. These declining trends were significantly less in the group treated with Benincasa cerifera compared with those in the I/R-only group (P =. 008, P =. 07, and P <. 001, respectively). Renal I/R produced a significant increase in malondialdehyde level, while pretreatment with Benincasa cerifera was associated with a significantly lower malondialdehyde level (P <. 001).Conclusions. These findings imply that reactive oxygen species play a crucial role in I/R-induced kidney injury and Benincasa cerifera exerts renoprotective activity probably by the radical scavenging activity.
  • Reza Afshar, Suzan Sanavi, Mohammad, Reza Jalali Nadooshan Pages 86-88
    Introduction. Exercise induces renal hemodynamic alterations and stimulates electrolytes excretion. The purpose of this study was to assess urinary excretion of sodium and potassium in karate practitioners, following competitions.Materials and Methods. The study population composed of 18 healthy men, aged 18 to 21 years, with similar physical characteristics. They were professional karatekas with a history of at least 7 years of karate training. The participants competed in 3 rounds of about 3 minutes in duration with 10 minutes resting intervals between them. The 24-hour urine samples were collected before (while trainings were stopped) and after the match and their sodium and potassium concentrations were measured. Also, blood samples were obtained before and after the match for measurement of these electrolytes in the participants’ sera.Results. Before the match, the mean values of urinary sodium and potassium were 200.3 +/- 89.3 mEq/L/d and 68.5 +/- 12.9 mEq/L/d, respectively. After the match, they changed into 206.9 +/- 74.7 mEq/L/d and 67.1 +/- 14.4 mEq/L/d, respectively. No significant alterations were observed in urinary sodium and potassium excretion following karate match (P =. 94 and P =. 96, respectively). Serum sodium levels were 136.7 +/- 3.1 mEq/L and 136.3 +/- 2.9 mEq/L, before and after the match, respectively (P =. 11), serum potassium levels were 4.2 +/- 0.3 mEq/L and 4.1 +/- 0.2 mEq/L, respectively (P =. 16).Conclusions. With regard to short duration and anaerobic nature of karate, it seems that a Karate match does not contribute to excessive urinary electrolytes excretion.
  • Masoumeh Mohkam, Fahimeh Asgarian, Alireza Fahimzad, Mostafa Sharifian, Reza Dalirani, Fatemeh Abdollah Gorgi Pages 89-92
    Introduction. Tumor necrosis factor-alpha (TNF-?) is an important mediator of the inflammatory response in serious bacterial infections. The aim of this study was to evaluate the potential of urinary TNF-? for diagnosis of acute pyelonephritis in children.Materials and Methods. This study was conducted from March 2006 to December 2007 on children with confirmed diagnosis of acute pyelonephritis. They all had positive renal scintigraphy scans for pyelonephritis and leukocyturia. The ratios of urinary TNF-? to urine creatinine level were determined and compared in patients before and after antibiotic therapy. Results. Eighty-two children (13 boys and 69 girls) with acute pyelonephritis were evaluated. The mean pretreatment ratio of urinary TNF-? to urinary creatinine level was higher than that 3 days after starting on empirical treatment (P =. 03). The sensitivity of this parameter was 91% for diagnosis of acute pyelonephritis when compared with demercaptosuccinic acid renal scintigraphy as gold standard. Conclusions. Based on our findings in children, the level of urinary TNF-?-creatinine ratio is acute increased in pyelonephritis and it decreases after appropriate therapy with a high sensitivity for early diagnosis of the disease. Further research is warranted for shedding light on the potential diagnostic role of urinary TNF-? in pyelonephritis in children.
  • Nadereh Rashtchizadeh, Hassan Argani, Amir Ghorbanihaghjo, Nariman Nezami, Javid Safa, Soheila Montazer, Saheb Pages 93-98
    Introduction. We aimed to evaluate the high-sensitivity C-reactive protein (HS-CRP) level changes at the beginning and after withdrawal of lovastatin therapy in patients with diabetic nephropathy. Materials and Methods. Thirty male patients with type 2 diabetes mellitus and diabetic nephropathy were enrolled in the study. Lovastatin, 20 mg/d, was administered for 90 days. Afterwards, Lovastatin was withdrawn for the next 30 days. Blood samples were obtained before the intervention, on the 90th day, and days 1, 7, and 30 after withdrawal of Lovastatin. Serum level of HS-CRP was determined by enzyme-linked immunosorbent assay. Alterations in lipid profile was assessed, as well, and compared with that of HS-CRP. Results. Serum level of HS-CRP was significantly reduced after 90 days of lovastatin therapy (P <. 001). Then, the HS-CRP reached the pretreatment baseline level on the 7th day after lovastatin withdrawal and maintained until the 30th day (P <. 001). Serum HS-CRP changes showed no significant association with lipid profile except for serum total cholesterol level (r = 0.9, P =. 006) after 3 months of lovastatin therapy. Their association was re-evaluated after 7 days and 1 month of treatment withdrawal and no significant correlations were found. Conclusions. Our findings suggest that lovastatin decreases serum CRP level in patients with diabetic nephropathy, and 7 days after lovastatin cessation, CRP level increases again.
  • Hasan Otukesh, Behzad Ghazanfari, Seyed, Mohammad Fereshtehnejad, Masoomeh Bakhshayesh, Mehrdad Hashemi, Rozita Hoseini, Majid Chalian, Arezoo Salami, Leila Mehdipor, Aysan Rahiminia Pages 99-102
    Introduction. Congenital nephrotic syndrome may be caused by mutations in NPHS1 and NPHS2, which encode nephrin and podocin, respectively. Since the identification of the NPHS2 gene, various investigators have demonstrated that its mutation is an important cause of steroid-resistant nephrotic syndrome. We aimed to evaluate frequency and spectrum of podocin mutations in the Iranian children with steroid-resistant nephritic syndrome. Materials and Methods. We examined 20 children with steroid-resistant nephritic syndrome referred to Ali Asghar Children’s Hospital, in Tehran, Iran. Mutations in the 5th and 7th exons of NPHS2 were assessed. The mutational analysis of NPHS2 was performed by DNA sequencing. Results. The mean age at the onset of proteinuria was 6.4 ± 3.6 years. None of the children had mutations in the exons 5 or 7. Conclusions. Our study suggests that NPHS2 mutations in exons 5 and 7 are not seen in our children. Therefore, we cannot recommend NPHS2 (exons 5 and 7) mutation for screening in Iranian children with steroid-resistant nephritic syndrome. Other exons of podocin or other podocyte proteins in Iranian children may play a role in pathogenesis of steroid-resistant nephritic syndrome.
  • Vahid Pourfarziani, Mohammad Hossein Nourbala, Mehdi Azizabadi Farahani, Maryam Moghani Lankarani, Shervin Assari Pages 103-108
    Introduction. We assessed the costs of hospital admissions and length of hospital stay in kidney allograft recipients admitted to our center, in order to rank hospitalization causes in terms of costly and prolonged admissions, to bring to light the respective correlates of costly and prolonged admissions, and to investigate the relationship between costs and length of rehospitalizations. Materials and Methods. In a retrospective study at Baqyiatallah Hospital, in Tehran, records of 358 posttransplant hospitalizations were reviewed for the costs and duration of hospital stay. The causes of rehospitalizations, relative frequency of prolonged stays in costly rehospitalizations, and also relative frequency of costly admissions in short and prolonged stays were evaluated.Results. Among rehospitalizations, 83.3% of those due to cerebrovascular accident were costly and 51% of those with graft rejection resulted in prolonged hospital stays. Costly admissions had a high regularity in cases of patients older than 60 years, end-stage renal disease due to diabetes mellitus, graft loss, intensive care unit admission, and hospitalizations accompanied by in death. Prolonged stays were more common in those who were admitted to intensive care unit and those who ultimately died. The Costs showed a significant correlation with the length of rehospitalization (r = 0.626, P =. 001). Conclusions. The strong correlation between the length of hospitalization and posttransplant hospitalization costs means that the former should be curtailed by focusing on such correlates of high-cost admissions as high age and diabetes mellitus as the cause of kidney failure.
  • Esmat Ghanei, Amirhossein Miladipour, Alireza Nasrollahi, Mohammad Homayuni Pages 109-111
    Brucellosis is a multisystem disease that may present with a broad spectrum of clinical manifestations. The most frequent symptoms are constitutional symptoms. While involvement of the bones, joints, and liver is not rare, brucellosis may rarely involve the kidney. We present a case of brucellosis with hepatitis, pancytopenia, peripheral arthritis, and kidney failure.
  • Fariba Samadian, Mahmoud Parvin, Amirhossein Faraji, Pedram Ahmadpoor Pages 112-113
  • Ali Zarei Mahmoudabadi, Ali Reza Keradmand, Nasim Enayatollahi Pages 114-115
  • Pages 116-117
  • Pages 118-119