cartas al director multinucleadas fue la característica histológica común. Cabe destacar la importancia de la biopsia renal ante casos de insuficiencia renal no justificada, y en el caso concreto de sospecha de sarcoidosis dada la variedad de lesiones que puede producir, la práctica de la biopsia optimizará la elección del tratamiento médico. 1. Casella FJ, Allon MJ. The kidney in sarcoidosis. Am Soc Nephrol 1993;3:1555-62. 2. Peces R, Laurés AS, Navascués RA, Baltar J, Seco M, Ortega F, et al. El espectro de afectación renal en la sarcoidosis: presentación de tres casos. Nefrologia 1998;18(2):161-4. 3. O’Riordan E, Willert RP, Reeve R, Kalra PA, O’Donoghue DJ, Foley RN, et al. Isolated sarcoid granulomatous interstitial nephritis. Review of five cases at one center. Clin Nephrol 2001;55:297-302. 4. Mignon F, Mery JP, Mougenot B, Ronco P, Roland J, Morel-Maroger L. Granulomatous interstitial nephritis. Adv Nephrol Necker Hosp 1984;13:219-45. 5. Joss N, Morris S, Young B, Geddes C. Granulomatous Interstitial Nephritis. Clin J Am Soc Nephrol 2007;2:222-30. 6. Picazo M, Cuxart M, Ballarín JA, Huerta MV. Diagnóstico de sarcoidosis a partir de un caso de insuficiencia renal aguda. Nefrologia 2006;26(5):631-2. 7. Ford MJ, Anderton JL, MacLean N. Granulomatous sarcoid nephropathy. Postgrad Med J 1978;54:416-7. 8. Robson MG, Banerjee D, Hopster D, Cairns HS. Seven cases of granulomatous interstitial nephritis in the absence of extrarenal sarcoid. Nephrol Dial Transplant 2003;18:280-4. M. Cuxart1, M. Picazo1, R. Sans Lorman1, M.J. Muntané2 1 Servicio de Nefrología. Hospital de Figueres. Figueres. Girona. 2 Servicio de Anatomía Patológica. Hospital de Figueres. Figueres. Girona. Correspondencia: M. Cuxart Servicio de Nefrología. Hospital de Figueres. Ronda Rector Arolas, s/n. 17600 Figueres. Girona.
[email protected] [email protected]
702
Acute phosphate nephropathy after bowel cleansing: still a menace Nefrologia 2010;30(6):702-4 doi: 10.3265/Nefrologia.pre2010.Jul.10544
Dear editor: Colonoscopy is critically dependent on adequate pre-procedural bowel cleansing and oral sodium phosphate bowel purgatives (OSP) have been used with good acceptance and efficacy for this purpose1. Among others metabolic and clinical disturbances described after the procedure, acute kidney injury may be a serious complication2,3. We present two cases of sodium phosphate induced acute renal failure. Case 1 A 84 year-old male with a past history of stage 3 obstructive chronic renal failure, prostatic hypertrophy and hypertension, medicated with losartan. presented with complaints of six months weigh loss and changed bowel habits. A colonoscopy was performed after preparation with oral sodium phosphate solution (Fleet phosphosoda®) with standard dose and its result was normal. A week later, the patient reported pedal and orbital oedema and was observed on the emergency department. The physical examination was unremarkable except for hypertension (180/80 mmHg) and lower limbs oedema. Laboratory results showed haemoglobin 11.1 g/dl, serum urea 346 mg/dl, serum crea-
Figure 1. Kidney biopsy. Von Kossa coloration (40x).
tinine 9.2 mg/dl, serum sodium 130 mEq/L, serum potassium 6.5 mEq/L, serum phosphorus 6.6 mg/dl, normal serum calcium, serum bicarbonate 15 mEq/L and mild proteinuria. Serum and urine immunoelectrophoresis and immunologic study were normal. Renal ultrasound showed increased cortical echogenicity. Haemodialysis was initiated. Kidney biopsy showed minimal mesangial expansion. The tubules were mildly dilated and focal interstitial fibrosis was present. Von Kossa stain positive deposits were observed within the cytoplasm of tubular epithelial cells, tubular lumen and interstitium. (figure 1 and figure 2) Immunofluorescence was negative for immunoglobulin or complement. We made the diagnosis of acute phosphate nephropathy secondary to administration of a sodium phosphate purgative. Renal dysfunction didn’t improve after 7 months and the patient continues on regular haemodialysis. Case 2 A 88 year-old male with a past history of prostatic hypertrophy and marginal zoneB cell lymphoma IV-B stage (treated with vincristine, cyclophosphamide and prednisolone for two cycles followed by second line therapy with rituximab and chlorambucil with disease progression) and stage 4 obstructive chronic renal failure. A virtual colonoscopy was performed after bowel preparation with Fleet phosphosoda®. Colonic diverticulosis was diagnosed. Five days latter the patient reported le-
Figure 2. Kidney biopsy. Von Kossa coloration (100x). Nefrologia 2010;30(6):698-713
cartas al director thargy and anuria and was admitted on the emergency department. He presented with drowsiness and was hypotensive, apyretic and oliguric. He presented inspiratory crackles on chest exam, distended and painful abdomen without guarding and lower limb oedema. Abnormal test results were hemoglobin 9.7 g/dL, leucocytes 17.1 x 109/L (87% neutrophils), platelets 70 x 109/L, serum creatinine 3.45 mg/dL, serum urea 106 mg/dL, serum calcium 4.5 mg/dl, serum phosphorus 18.3 mg/dL, lactate dehydrogenase 3,028 U/L, C-reactive protein 28.2 mg/dL, pH 7.3, bicarbonate 13.3 mEq/L and lactate 7.5 mmol/L; Urine dipstick was positive for blood, leucocytes and proteins. Renal ultrasound showed kidneys with enhanced echogenicity. Chest radiograph showed interstitial oedema and abdominal radiograph was normal. Suspected severe urinary sepsis and acute kidney injury secondary to sepsis and phosphate nephropathy were assumed. Intravenous fluid was started, samples were obtained for culture and broad spectrum antibiotics were started. There was no clinical improvement and conservative measures were adopted. DISCUSSION Acute phosphate nephropathy (AphN) is a form of kidney injury that occurs after the use of bowel purgatives that contain oral sodium phosphate (OSP)2. OSP bowel solution (Fleet phosphosoda®) is a hyperosmotic purgative that has been used with good acceptance and efficacy in bowel cleansing before colonoscopy1. Both patients made the standard regimen (two 45 ml doses taken 10-12 h apart). Each dose contains monobasic and dibasic sodium phosphate providing the equivalent of 5,8 g of elemental phosphorus and 5 g of sodium3. Intestinal absorption occurs and transient hyperphosphatemia and hypocalcemia are found in all patients2. However, severe hyperphosphatemia, symptomatic hypocalcemia, hypernatremia, symptomatic hyponatremia, hypokalemia, anion-gap acidosis and acute kidney injury have been described after the procedure3-6. Two different Nefrologia 2010;30(6):698-713
clinical patterns of OSP-induced acute kidney injury have been described: early symptomatic and late insidious2. The earlier form consists in an acute illness that manifests as changes in mental status, tetany, or cardiovascular collapse, usually in hours of bowel preparation, and patients present with severe hyperphophatemia and hypocalcemia. The second patient presented fit in this category. These patients require urgent fluid resuscitation, rapid correction of electrolyte disturbances, and sometimes dialysis. Despite aggressive fluid replacement and resuscitation our patient died. Some patients with this presentation survive and show renal function recovery2. The second form is due to AphN with a more insidious onset (days to months) and is generally irreversible1. At the time of diagnosis, serum phosphorus and calcium levels are normal, unless measured within 3 days of bowel preparation. This was in fact the case of the first patient. As we found, the main pathologic finding in kidney biopsy is nephrocalcinosis demonstrated with the Von Kossa stain1. Following reports of AphN Fleet phosphosoda® was voluntary withdrawn from US market in 200810. However OSP solution is still in use in some countries, as Portugal. The pathophysiology of APhN involves transient hyperphospatemia, volume depletion exacerbated by concurrent ACEI, ARB and diuretics, and elevated distal tubular phosphate and calcium concentrations1,8,10. Risk factors include advanced age, chronic kidney failure, dehydratation, female gender, diuretics, a history of colitis, and, probably, diabetes mellitus and non-steroidal anti-inflammatory drugs1,10. Data indicate a high risk for chronic renal failure1,9,10. Our first patient needed long term haemodialysis. In Markowitz series none patient returned to their baseline creatinine levels and 19% progressed to ESRD at mean of 13.8 months after colonoscopy9. In conclusion, these cases highlight the importance of AphN because such OSP
are still used in clinical practice. Clinical presentation may assume two forms and, in any of these, consequences are serious and sometimes fatal. Strategies to prevent the development of APhN should be adopted and include avoidance in highrisk patients, adequate hydratation, dose minimization, increasing the interval between doses and possibly not administering ACE-I, ARB, diuretics and NSAID on the day before and the day after colonoscopy procedure6,10. It is also advisable to perform serum biochemistry tests after the procedure, in order to detect any renal or electrolyte abnormalities7. 1. Tan JJ, Tjandra JJ. Which is the optimal bowel preparation for colonoscopy-a meta-analysis. Colorectal Dis 2006;8(4):247-58. 2. Lien YH. Is bowel preparation before colonoscopy a risky business for the kidney? Nat Clinl Pract Nephrol 2008;4(11):606-14. 3. Heher EC, Their SO, Rennke H, Humphreys BD. Adverse renal and metabolic effects associated with oral sodium phosphate bowel preparation. Clin J Am Soc Nephrol 2008;3(5):1494503. 4. Bennouna M, Anaya S, De la Nieta DS, Rivera F. Enema in a patient with renal failure: a cause of severe hyperphosphatemia. Nefrologia 2008;28(6):657-9. 5. Hurst FP, Boehn EM, Osgard EM, Oliver DK, Das NP, Gao SW. Association of oral sodium phosphate purgative use with acute kidney injury. J Am Soc Nephrol 2007;18(12):3192-8. 6. Frizelle FA, Colls BM. Hyponatremia and seizures after bowel preparation: Report of three cases. Dis Colon Rectum 2005;48(2):393-6. 7. Desmeules S, Bergeron MJ, Isenring P. Acute Phosphate Nephropathy and renal failure. N Eng J Med 2003;349(10):1006-7. 8. Markowitz GS, Nasr SH, Klein P, Anderson H, Stack JI, Alterman L et al. Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleasing. Human Pathol 2004;35(6):675-84. 9. Markowitz GS, Stokes BM, Radhakrishnan J, D’Agati VD. Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure. J Am Soc Nephrol 703
cartas al director 2005;16(11):3389-96. 10. Markowitz GS, Perazella MA. Acute phosphate nephropathy. Kidney Int 2009;76(10):1027-34.
P. Santos1, A. Branco1, S. Silva1, A. Paiva1, J. Baldaia1, J. Maximino1, A. Loureiro1, R. Henrique2 1 Nephrology Unit. Internal Medicine Department. Pedro Hispano Hospital. Matosinhos (Portugal). 2 Department of Pathology. Portuguese Institute of Oncology. Porto (Portugal). Correspondence: P. Santos Nephrology Unit. Internal Medicine Department. Pedro Hispano Hospital. Matosinhos. Portugal.
[email protected]
Infección por parvovirus B19: diagnóstico y tratamiento en un paciente sometido a trasplante renal Nefrologia 2010;30(6):704 doi:10.3265/Nefrologia.pre2010.Jul.10429
Sr. Director: Se sabe que la incidencia de enfermedad por parvovirus B19 tiene una in cidencia del 2% después del trasplante de órganos sólidos. El parvovirus B19 es un eritrovirus de la familia Parvoviridae que se replica preferentemente en los precursores de los eritrocitos humanos. Clínicamente se presenta con fiebre, artralgias y exantema en un 25, 7 y 6%, de los casos, respectivamente, y la anemia es el signo de mayor expresión en los pacientes (99%). No puede confiarse en el diagnóstico de la infección por serología (IgM e IgG) debido a la demora e inadecuada respuesta inmune mediada por anticuerpos en inmunocomprometidos. El uso de reacción de cadena de polimerasa (PCR) mejoró la detección de infección por parvovirus B19, y su valor predictivo positivo de PCR positiva en huésped inmunocomprometido es mayor cuando se acompa704
ña de aplasia de células rojas. Si la serología y la PCR son negativas, el estudio de la médula ósea con hibridación in situ e inmunohistoquímica podrían aclarar el diagnóstico. No existe en la actualidad descripción de tratamientos con fármacos antivirales. Sin embargo, pudo demostrarse un efecto beneficioso de las inmunoglobulinas administradas a altas dosis (IVIG) en receptores de trasplante renal para dicha infección. La dosis óptima y el tiempo de la terapia no se han establecido, ya que algunos pacientes requieren cursos adicionales del fármaco. Además, es prioritario disminuir la inmunosupresión. Se describe el caso de un paciente hombre de 36 años de edad con diagnóstico de insuficiencia renal crónica de etiología desconocida. Ingresa para hemodiálisis en 2008 y posteriormente recibe trasplante renal de donante cadáver de 9 años de edad con antecedente de traumatismo craneoencefálico (TEC), en enero de 2010. Recibe tratamiento de inducción con timoglobulina, corticoides y micofenolato sódico. El mantenimiento se lleva a cabo con tacrolimus, deltisona y micofenolato sodico. Recibe profilaxis con ganciclovir para citomegalovirus (CMV) y trimetoprima-sulfametoxazol (TMP-SMXZ) para PCP. Presenta como complicación, al tercer día posterior al trasplante, una fístula urinaria, corregida quirúrgicamente. Dos semanas después de este evento cursa con síndrome diarreico asociado a micofenolato y anemia severa (Hcto 19%) normocítica, normocrómica con reticulopenia, sin alteraciones en la serie de glóbulos blancos y plaquetas Coombs negativas. Presenta un alto requerimiento de transfusiones por síndrome anémico sintomático. En febrero de 2010 presenta síndrome febril e infección urinaria por Acinetobacter sp., por lo que recibe por sensibilidad tratamiento con amikacina. El paciente continúa con síndrome anémico con las mismas caracteristicas descritas, asociado con artralgias y mialgias. Se solicita perfil ferrocinético con parámetros normales. Se aumenta la dosis máxima de eritropoyetina, sin respuesta. Se evalúan: SOMF y examen parasitológico
seriado de materia fecal, que fueron negativos. Se realizan endoscopia alta y baja sin evidencia de hemorragia, vídeo por endocápsula: s/p, evaluación hematológica con frotis y PAMO: hipoplasia de serie eritroide sin alteraciones de serie blanca y plaquetas. Dosaje de anticuerpos IgG e IgM para parvovirus B19 negativos y PCR para parvovirus B19 positiva. Se indica tratamiento con IVIG 400 mg/kg/día (30 g/día) durante 5 días. Se suspende el micofenolato sódico. La función renal se mantiene estable (creatininas promedio 1,4 mg/dl); 10 y 14 días después del tratamiento presenta aumento del Hcto (35 y 38%) y reticulocitos. La PCR para parvovirus de control (8 semanas posteriores al tratamiento) es negativa. Se mantiene la inmunosupresion con tacrolimus y deltisona. Se seguirá con controles periódicos con ADN-PCR. 1. Eid A, et al. Parvovirus B19 in Solid Organ Transplant Recipients. Am J Transplant 2009;9(Suppl 4):S147-S150. 2. Manaresi E, et al. Diagnosis and quantitative evaluation of parvovirus B19 infections by realtime PCR in the clinical lab. J Med Virol 2002;67:275-81. L.R. León, D. Curcio, D. Casadei Servicio de Nefrología y Trasplante Renal. Nephrology S.A. Caba. Buenos Aires (Argentina) Correspondencia: L.R. León Servicio de Nefrología y Trasplante Renal, Nephrology S.A., Cabello 3889, 1425, Caba, Buenos Aires, Argentina.
[email protected]
Tuberculosis diseminada con abscesos esplénicos en hemodiálisis Nefrologia 2010;30(6):704-6 doi:10.3265/Nefrologia.pre2010.Aug.10617
Sr. Director: Los pacientes en hemodiálisis presentan mayor predisposición al desarrollo de infecciones por la existencia de alteNefrologia 2010;30(6):698-713
