| Abstract|| |
To determine the conditions that result in pediatric nephrology consultations in an academic hospital setting, we studied 178 prospective consecutive consultations for 125 inpatients (69 boys and 56 girls) at the Jordan University Hospital, Amman, Jordan from January 2006 to December 2006. The mean age at the time of consultation was 3.1 years (median of 1 year, and range from 1 day to 16 years). Of the 125 patients, 87 (69.6%) patients had a single consultation, while 38 (30.4%) patients had multiple encounters (range from 1-4 consultations). The reasons for consultations included fluids and electrolytes imbalances (29.0%), hydronephrosis (15.7%), urinary tract infections (14.2%), acute renal failure (ARF) (14.2%), hypertension (8.40%), and miscellaneous conditions (18.5%). The most frequent fluids and electrolyte disorders were polyuria, hypocalcemia, and hyponatremia. Routine administration of hypotonic intravenous fluids was a major contributory factor to hyponatremia. The most frequent cause of ARF was acute tubular necrosis in association with multiple organ dysfunction and antibiotic nephrotoxicity. Hypertension was mostly neurogenic in origin.
Keywords: Pediatric, Renal, Failure, Electrolytes, Hypertension, Nephrotoxicity, Hydronephrosis, Urinary, Infections, Jordan, Consultations
|How to cite this article:|
Akl K. Pediatric Nephrology Consultations in a Tertiary Academic Center in Jordan. Saudi J Kidney Dis Transpl 2008;19:456-60
| Introduction|| |
Consultations form an integral part of the pediatric nephrology service. It serves as a teaching experience for the resident, fellow, and consultant alike. The purpose of this prospective study is to demonstrate the prevalent reasons for pediatric nephrology consultations in a tertiary academic center in Jordan.
| Patients and Methods|| |
We studied 178 prospective consecutive pediatric nephrology consultations for 125 inpatients (69 boys and 56 girls) at the Jordan University Hospital from January 2006 to December 2006. The consults covered patients on the wards and intensive care units (pediatric, neonatal, surgical, and neurosurgical). We excluded outpatient consultations from this study. The patients were followed up from 1 day to 14 months.
We defined acute renal failure (ARF) as an abrupt decline in glomerular filtration rate, hyponatremia as serum sodium < 135 mmol/ L, severe hyponatremia as serum sodium < 120 mmol/L, polyuria as urine output > 3 ml/ kg/hour, multiple organ dysfunction syndrome (MODS) as simultaneous dysfunction lasting at least 24 to 48 hours of at least 2 organ systems other than the one with which patient was admitted, , hydronephrosis as dilatation of the renal pelvis, hypertension as systolic blood pressure and/or diastolic blood pressure that is > 95 th percentile on repeated measurement,  recurrent urinary tract infections as > 3 episodes per year, and sepsis as documented infection with complex activation of the immune system.
| Results|| |
The mean age of patients was 3.1 years at the time of consultation (range from 1 day to 16 years). A total of 87 (69.6%) patients had a single consultation, while 38 (30.4%) patients had multiple encounters (range from 1 to 4 consultations).
Fluids and electrolyte disorders were the reasons for 52 (29.0%) consultations, which comprised polyuria in 12 cases, hypocalcemia in 8, hyponatremia in 6, metabolic acidosis in 6, edema in 5, hypernatremia in 5, and hypokalemia in 3, ascites in 2, pulmonary edema in 2, hyperkalemia in 2, and hypercalcemia in 1. Hyponatremia was associated with chronic pneumonia in 2 cases, marked fluid overload in 1, polyuria in1, Hirschsprungs disease in 1, and MODS in 1. Such patients precipitated hyponatremia mostly by i.v. hypotonic solutions.
Antenatal hydronephrosis was the reason for 28 (15.7%) consultations; 11 cases of idiopathic hydronephrosis, 5 neurogenic bladders secondary to myelomeningocele, 4 vesicoureteral reflux (VUR), 3 imperforate anus, 3 pelviureteric junction obstruction requiring surgery, and 2 posterior urethral valve.
Urinary tract infection (UTI) was the reason for 25 (14.2%) consultations; isolated UTI in 18 cases, acute pyelonephritis (APN) associated with hydronephrosis in 2, part of sepsis in 2, isolated APN in 1, APN associated with VUR in 1, and acute lobar nephronia in 1.
ARF was the reason for 25 (14.2 %) consultations. It was associated with MODS in 11 cases, drug nephrotoxicity in 4 (gentamicin, acyclovir, vancomycin, and furosemide), prerenal in 4 hypernatremia in 3, rapidly progressive glomerulonephritis in 1, lupus nephritis in 1, and partial hemolytic uremic syndrome in 1.
Hypertension was the reason for 15 (8.4%) consultations; neurogenic in 7 cases, renoparenchymal disease in 3, idiopathic in 2, fluid overload in 1, hydronephrosis in 1, and rapidly progressive glomerulonephritis in 1.
Finally, miscellaneous conditions were the reason for 33 (18.5%) of consultations; hematuria in 6 cases, vesicoureteral reflux in 5, laboratory abnormalities in 4, choice of drug/ fluid in 3, rickets in 3, renal cyst in 2, nephrotic syndrome in 2, dysuria in 2, enuresis in 1, workup for systemic lupus in 1, peritoneal dialysis in 2, urine retention in 1, and decreased urine output in 1.
| Discussion|| |
The clinical consultations we encountered in the pediatric patients in our tertiary center included fluids and electrolyte disorders, hydronephrosis, urinary tract infections, acute renal failure, hypertension, and several miscellaneous conditions.
A common electrolyte disorder in the pediatric intensive care unit (PICU) is hyponatremia which is the most common electrolyte disorder in hospitalized patients.  The most common cause is use of hypotonic intravenous fluids instead of isotonic ones. ,,,, This was the major contributing factor to hyponatremia and polyuria in our patients because of the traditional use of hypotonic intravenous fluids in the PICU. One of the most challenging situations in the PICU is differentiating between hyponatremia due to syndrome of inappropriate anti-diuretic hormone secretion (SIADH ), which is a volume expanded condition, and cerebral salt wasting (CSW), which is a volume contracted state.  Differentiating between euvolemia and hypovolemia can be clinically difficult even when plasma osmolality is measured. ,
Error in the diagnosis may be catastrophic as the treatment of each is the opposite of the other. Hospital mortality is higher in the presence of hyponatremia. ,,,, One out of the two patients who had pulmonary edema without renal or heart failure had hyponatremic encephalopathy. This association has been described before. 
Idiopathic antenatal hydronephrosis was the most common etiology of neonatal hydronephrosis. It is usually benign.  However, there is a risk of postnatal pathology in mild as well as moderate and severe antenatal hydronephrosis.  In cases of hydronephrosis with major anatomical abnormalities, severe vesicoureteral reflux, and neurogenic bladder, the use of antibiotic prophylaxis did not prevent recurrent urinary tract infections in our. Garin et al, demonstrated in a randomized controlled study no benefit from prophylactic antibiotics.  A systematic review had similar conclusion. 
The most common cause of ARF in the PICU was acute tubular necrosis associated with MODS and antibiotic nephrotoxicity. The majority of cases of ARF were associated with MODS that resulted in 100 % mortality. There was no benefit from the use of low dose dopamine , or diuretics.  Mortality increases when ARF is associated with MODS,  sepsis, ,, shock,  ventilator associated pneumonia, and antibiotic nephrotoxicity.  Nephrotoxic ARF is common in the neonatal intensive care unit.  Monitoring drug levels of aminoglcoside decreases the incidence of ARF, and once daily dosing is safer.  Prolonged recovery from vancomycin nephrotoxicity may be due to either acute interstitial nephritis or acute tubular necrosis. ,
Bunchman et al reported 49 %mortality rate in children with ARF undergoing PD.  Nonoliguric ARF has better prognosis than oliguric ARF.  However, since ARF is usually multifactorial, even nonoliguric ARF may be associated with high mortality.
The majority of our patients had neurogenic hypertension. Besides the baroreceptor and macula densa mechanisms, renin secretion is also regulated by the sympathetic nervous system. The brain has its own renin angiotensin system. Angiotensin IV, may cause hypertension, which does not respond to angiotensin converting enzyme inhibitors. However, it normalizes with angiotensin II receptor blockers. 
| References|| |
|1.||Doughty LA, Kaplan SS, Carcillo JA. Inflammatory cytokine and nitric oxide responses in pediatric sepsis and organ failure. Crit Care Med 1996;24(7):1137-43. |
|2.||Cengiz P, Zimmerman JJ. Prelude to pediatric multiple organ dysfunction syndrome: The golden hours concept revisited. Pediatr Crit Care Med 2003;4(2):263-4. |
|3.||The Fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics 2004;114(2):555-76 . |
|4.||Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatremia in hospitalized patients: Treatment-related risk factors and inadequate management. Nephrol Dial Transplant 2006;21(1):70-6 . |
|5.||Choong K, Kho ME, Menon K, Bohn D. Hypotonic versus isotonic saline in hospitalized children: A systematic review. Arch Dis Child 2006;91(10):828-35. |
|6.||Neville KA, Verge CF, Rosenberg AR, OMeara MW, Walker JL. Isotonic is better than hypotonic saline for intravenous rehydration in children with gastroenteritis: A prospective randomized study. Arch Dis Child 2006;91(3):226-32. |
|7.||Hoorn EJ, Geary D, Robb M, Halperin ML, Bohn D. Acute hyponatremia related to intravenous fluid administration in hospitalized children: An observational study. Pediatrics 2004;113(5):1279-84. |
|8.||Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: A case for using isotonic saline. Pediatrics 2003;111 (2):227-30. |
|9.||Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children. Pediatr Nephrol 2005;20(12): 1687-700. |
|10.||Boluyt N, Bollen CW, Bos AP, Kok JH, Offringa M. Fluid resuscitation in neonatal and pediatric hypovolemic shock: A Dutch Pediatric Society evidence-based clinical practice guideline. Intensive Care Med 2006;32(7):995-1003. |
|11.||Cole CD, Gottfried ON, Liu JK, Couldwell WT. Hyponatremia in the neurosurgical patient: Diagnosis and management. Neurosurg Focus 2004;16(4):E9. |
|12.||Palmer BF. Hyponatremia in patients with central nervous system 112-disease: SIADH versus CSW. Trends Endocrinol Metab 2003;14(4):182-7 . |
|13.||Jimenez R, Casado-Flores J, Nieto M, Garcia-Teresa MA. Cerebral salt wasting syndrome in children with acute central nervous system injury. Pediatr Neurol 2006;35(4):261-3 . |
|14.||Gill GV, Huda B, Boyd A, et al. Characteristics and outcome of severe hyponatremia: A Hospital- based study. Clin Endocrinol (Oxf) 2006;65(2):246-9 . |
|15.||Asadollahi K, Beeching N, Gill G. Hyponatremia as a risk factor for hospital mortality. QJM 2006;99(12):877-80 . |
|16.||Arief AI. Management of hyponatremia. BMJ 1993;307(6899):305-8 . |
|17.||Chung HM, Kluge R, Schrier RW, Anderson RJ. Postoperative hyponatremia: A prospective study. Arch Intern Med 1986;146 (2):333-6. |
|18.||Ayus JC, Arieff AI. Pulmonary complications of hyponatremic encephalopathy: Noncardiogenic pulmonary edema and hyperapnic respiratory failure. Chest 1995; 107(2):517-21 . |
|19.||Sidhu G, Beyene J, Roseblum ND. Outcome of isolated antenatal hydronephrosis: A systematic review and meta-analysis. Pediatr Nephrol 2006;21(2):218-24. |
|20.||Lee RS, Cendron M, Kinnamon DD, Nguyen HT. Antenatal hydronephrosis as a predictor of postnatal outcome: A metaanalysis. Pediatrics. 2006;118(2):586-93 . |
|21.||Garin EH, Olavarria F, Garcia Nieto V, Valenciano B, Campos A, Young L. Clinical significance of primary vesico-ureteral reflux and urinary antibiotic prophylaxis after acute pyelonephritis: A multicenter, randomized, controlled study. Pediatrics 2006; 117(3):626-32 . |
|22.||Williams GJ, Wei L, Lee A, Craig JC. Long-term antibiotics for preventing recurrent urinary tract infection in children. Cochrane Database Sys Rev 2006;3:CD001534. |
|23.||Friedrich JO, Adhikari N, Herridge MS, Beyene J. Meta-analysis: Low-dose Dopamine increases urine output but does not prevent renal dysfunction or death. Ann Intern Med 2005;142(7):510-24 |
|24.||Kellum JA, M Decker J. Use of dopamine in acute renal failure: A meta-analysis. Crit Care Med 2001;29(8):1526-31. |
|25.||Kellum JA. The use of diuretics and dopamine in acute renal failure: A systematic review of the evidence. Crit Care 1997;1(2):53-9. |
|26.||Khilnani P, Sarma D, Zimmerman J. Epidemiology and peculiarities of pediatric multiple organ dysfunction syndrome in New Delhi, India. Intensive Care Med 2006;32(11):1856-62 |
|27.||Riedemann N, Guo RF, Ward PA. The enigma of sepsis. J Clin Invest 2003;112 (4):460-7. |
|28.||Rangel-Fausto MS, Pittet D, Costigan M, Hwang T, Davis CS, Wenzel RP. The natural history of the systemic inflammatory response (SIRS): A prospective study. JAMA 1995;273(2):117-23. |
|29.||Neveu H, Kleinknecht D, Brivet T, Loirat P, Landais P. Prognostic factors in acute renal failure due to sepsis. Result of a prospective multicentre study: The French study Group on acute renal failure. Nephrol Dial Transplant 1996;11(2):293-9. |
|30.||Plotz FB, Hulst HE, Twisk JW, Bokenkamp A, Markhorst DG, van Wijk JA. Effect of acute renal failure on outcome in children with severe septic shock. Pediatr Nephrol 2005;20(8):1177-81. |
|31.||Gursel G, Demir N. Incidence and risk factors for the development of acute renal failure in patients with ventilator-associated pneumonia. Nephrology (Carlton) 2006;11 (3):159-64. |
|32.||Adelman RD, Wirth F, Rubio T. A controlled study of the nephrotoxicity of mezlocillin and amikacin in the neonate. Am J Dis Child 1987;141(11):1175-8. |
|33.||Contopoulos-Ioannidis DS, Giotis ND, Baliasta DV, Ioannidis JP. Extended interval aminoglycoside administration for children: A meta-analysis. Pediatrics 2004;114(1): e111-8. |
|34.||Codding CE, Ramseyer L, Allon M, Pitha J, Rodriguez M. Tubulointerstitial nephritis due to vancomycin. Am J Kidney Dis 1989; 14(6):512-5. |
|35.||Wicklow BA, Ogborn MR, Blydt-Hansen TD. Biopsy-proven acute tubular necrosis in a child attributed to vancomycin intoxication. Pediatr Nephrol 2006;21(8):1194-6 . |
|36.||Bunchman TE, McBryde KD, Mottes TE, Gardner JJ, Maxvold NJ, Brophy PD. Pediatric acute renal failure: Outcome by modality and disease. Pediatr Nephrol 2001;16(12):1067-71 . |
|37.||Stapleton FB, Jones DP, Green RS. Acute renal failure in neonates: Incidence, etiology and outcome. Pediatr Nephrol 1987;1(3):314-20. |
|38.||Lochard N, Thibault G, Silversides DW, Touyz M, Reudelhuber TL. Chronic production of angiotensin IV in the brain leads to hypertension that is reversible with an angiotensin II A T 1 receptor antagonist. Circ Res 2004;94(11):1451-7. |
Consultant Pediatric Nephrology, Assistant Professor of Pediatrics, Jordan University Hospital, P.O. Box 831373, Amman 11183