Hypertension, erythrocyturia and proteinuria in childhood non‐Hodgkin’s lymphoma

Olowu, Wasiu A.; Adelusola, Kayode A; Senbanjo, Idowu O; Adenowo, Olusola A; Badmos, KB

doi:10.1111/j.1440-1797.2006.00568.x

Cited by 4 publications

(8 citation statements)

References 23 publications

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“…Earlier reports on BLN have demonstrated urinalysis evidence of glomerulonephritis and glomerular and tubulointerstitial pathology [4,7]. In these reports, autopsy findings showed pale, massively enlarged kidneys with foci of petechial haemorrhages on the cortical surfaces [4,7]. In this patient, there was a more than 3-fold increase in the left kidney volume from baseline by ultrasound within 24 h. This represented a phenomenal growth that weighed heavily in favour of BLN among all other differential diagnoses.…”

Section: Commentarymentioning

confidence: 81%

“…This explains why the initial diagnosis in this 11-year-old boy was nephroblastoma despite the fact that the latter is rare in this age group [8]. In BL nephropathy (BLN), renal function perturbation may be rapidly progressive, leading to severe morbidities and renalfailure death within days, as lymphomatous infiltration of the kidney is usually very extensive [4,7]. Earlier reports on BLN have demonstrated urinalysis evidence of glomerulonephritis and glomerular and tubulointerstitial pathology [4,7].…”

Section: Commentarymentioning

confidence: 87%

“…With or without HTN, the few reported cases of BL-related nephropathy were bilateral nephropathies [4,5,6,7]. Unilateral nephromegaly with HTN due to BL has not been previously reported.…”

Section: Commentarymentioning

confidence: 90%

“…In BL nephropathy (BLN), renal function perturbation may be rapidly progressive, leading to severe morbidities and renalfailure death within days, as lymphomatous infiltration of the kidney is usually very extensive [4,7]. Earlier reports on BLN have demonstrated urinalysis evidence of glomerulonephritis and glomerular and tubulointerstitial pathology [4,7]. In these reports, autopsy findings showed pale, massively enlarged kidneys with foci of petechial haemorrhages on the cortical surfaces [4,7].…”

Section: Commentarymentioning

confidence: 95%

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Stage 2 hypertension in a child with a rapidly enlarging kidney: answer

Olowu

Adelusola

2008

Pediatr Nephrol

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Answers1. Burkitt's lymphoma (BL) is the most likely aetiology, especially in an endemic region. BL is a nonmetastatic, highly proliferative, multicentric tumour. It is the fastest growing tumour in humans, with a doubling rate of 24 h [2]. 2. These will include nephroblastoma, acute unilateral obstructive uropathy and renal vein thrombosis. 3. Confirmation is either by fine-needle aspirate of the tumour for cytology or renal biopsy for histopathology. Both procedures confirmed BL on admission day 4 ( Fig. 1a). There was also glomerular evidence of proliferative glomerulonephritis with Bowman's capsule ruptures and tuft adhesions (Fig. 1b). Renal biopsy findings at 4 weeks are shown in Fig. 1c. 4. It is possible that the extensive renal infiltration by Burkitt's tumour with glomerulotubular compression and destruction (Figs. 1a-c), glomerulonephritis and enhanced renin-angiotensin-aldosterone-system (RAAS) activity played dominant roles in the causation of hypertension (HTN) in this patient. The proteinuria could have been due to the combination of glomerulonephritis and systemic and intraglomerular HTN brought about by increased RAAS activity. HTN may cause high glomerular filtration pressure in both kidneys with resultant proteinuria. Hypernatraemia, hypokalaemia, avid tubular sodium reabsorption and kaliuresis suggest enhanced RAAS activity in the patient. 5. BL is highly responsive to cytotoxic drugs. Tumour remission was induced with low-dose cyclophosphamide infusion, 125 mg/m 2 /48 h for four doses [3]. He also received antitumour lysis syndrome regimen, including allopurinol [3]. Significant reduction in the renal mass occurred within 72 h of cyclophosphamide infusion. Tumour remission was subsequently maintained with cycles of combination chemotherapy that comprised cyclophosphamide 1,000 mg/m 2 /dose, methotrexate 75 mg/m 2 /dose and vincristine 1.5 mg/m 2 /dose as stat intravenous doses. Intrathecal (IT) methotrexate 12.5 mg/m 2 on chemotherapy days 1 and 8, and IT cytosine arabinoside 50 mg/m 2 on day 4 were also given. The cycle was repeated fortnightly after ensuring normal blood counts. Overall, he received only three of six prescribed cycles because he was immediately lost to follow-up after hospital discharge. His hypertension was appropriately treated with parenteral hydralazine, frusemide, oral spironolactone and lacidipine. BP normalised (100/60 mmHg) by day 10 of induction chemotherapy. The antihypertensives were subsequently discontinued without adverse events. 6. Given the severity of the glomerular lesion that included Bowman's capsule ruptures with interstitial communications (Fig. 1b) and tuft synechiae as shown in the histopathology of the second renal biopsy (Fig. 1c), progression to chronic renal failure is a potential complication.

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Section: Commentarymentioning

confidence: 81%

Section: Commentarymentioning

confidence: 87%

“…With or without HTN, the few reported cases of BL-related nephropathy were bilateral nephropathies [4,5,6,7]. Unilateral nephromegaly with HTN due to BL has not been previously reported.…”

Section: Commentarymentioning

confidence: 90%

Section: Commentarymentioning

confidence: 95%

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Stage 2 hypertension in a child with a rapidly enlarging kidney: answer

Olowu

Adelusola

2008

Pediatr Nephrol

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“…Embryonal RMS occurs most commonly in children [3,4], and nearly 80% of genitourinary tract RMS is embryonal in nature [5]. While some malignancies have been associated with nephrotic syndrome (NS) [6][7][8][9][10], that occurring in association with RMS is very rare [11]. In this report, we present a case of nephrotic focal segmental glomerulosclerosis (FSGS) that was associated with embryonal RMS of the sarcoma botryoides subtype.…”

Section: Introductionmentioning

confidence: 90%

Focal segmental glomerulosclerosis and nephrotic syndrome in a child with embryonal rhabdomyosarcoma

et al. 2008

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A case of nephrotic syndrome (NS) and acute renal failure (ARF) associated with embryonal rhabdomyosarcoma (RMS) in a 10-year-old boy is reported. Ultrasound revealed irregular, echogenic, circumferential urinary bladder base mass, bilateral hydroureter and hydronephrosis. Histopathology of percutaneous renal and urethrocystoscopic biopsy specimens, respectively, revealed focal segmental glomerulosclerosis (FSGS) and embryonal RMS. Tumour remission was induced with pulse doses of intravenous vincristine, cyclophosphamide, methotrexate and actinomycin D over a 15-month period. He has been followed-up for 28 months and has maintained a drug-free tumour and proteinuria remission for 1 year. While some malignancies have been reported in association with NS, its occurrence in association with RMS is quite exceptional. We conclude that RMS may be associated with FSGS and NS. Effective treatment of the RMS was associated with sustained remission of the nephrotic proteinuria.

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Stage 2 hypertension in a child with a rapidly enlarging kidney: question

Olowu

Adelusola

2008

Pediatr Nephrol

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Case summarySevere headache, vomiting, and blurred vision preceded confusion, irrational behaviours and afebrile generalized tonic-clonic seizures by 3 days in this 11-year-old boy. All four seizure episodes occurred within 24 h and before hospital arrival. Each episode lasted 3-5 min. A progressively increasing painless left abdominal swelling preceded all these complaints by 3 weeks. There were no urinary symptoms. He was neither tremulous nor sweating excessively.The patient was drowsy, with a Glasgow coma score of 10/15. There was neither neck stiffness nor positive Kerning's sign. Muscle tone and tendon reflexes were normal. His blood pressure (BP), 160/120 mmHg (mean arterial pressure, 133 mmHg), was in the stage 2 hypertension (HTN) range (> 5 mmHg above the 99th percentile for age, gender and height [1]). There was no femoral pulse delay. Temperature, pulse and respiratory rate were 36.5°C, 96 beats/min, and 26 cycles/min, respectively. He was neither pale, dehydrated nor dyspnoeic. There was no papilloedema. Skin lesions suggestive of neurofibromatosis or systemic lupus erythematosus were absent. There was generalized discrete, painless, significant peripheral lymphadenopathy. Moderate ascites was present, but no peripheral oedema. The left kidney was markedly enlarged, but the right kidney was not palpable. Spleen and liver were not palpable. He had no abdominal bruit. His weight, height and body mass index were 28.0 kg, 131.0 cm and 16.32 kg/m 2 , respectively. Table 1 shows the results of biochemical and renal ultrasound investigations at baseline and at 4 weeks. Pretreatment haematocrit was 34.0%; white blood cell count, differentials, and platelets count were within normal limits. Haemoglobin electrophoresis was AS. Serology was negative for hepatitis B and C viruses and human immunodeficiency virus. Figure 1a shows a remarkably enlarged hypoechoic left kidney, with loss of corticomedullary differentiation. The right kidney was normal (Fig. 1b). The ultrasound was repeated 24 h later when an increase in the left kidney size was clinically observed as a posterior bulge in the lumbar region. It revealed a more than threefold increase in the kidney volume (Table 1, footnote a). Right kidney dimensions remained unchanged. Cerebrospinal fluid and bone marrow examinations were normal. The provisional diagnosis was nephroblastoma. The final diagnosis, however, turned out not to be nephroblastoma. His response to definitive treatment was good. He was discharged home for completion of treatment as outpatient on admission day 45 but was immediately lost to follow-up. His discharge BP was 90/60 mmHg.The answer to this question can be found at http://dx.

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Hypertension, erythrocyturia and proteinuria in childhood non‐Hodgkin’s lymphoma

Abstract: We conclude that all the children with BNHL/ARF had enlarged kidneys and evidence of glomerular disease. The mechanism of the glomerular disease is unclear. It is associated with a high mortality rate.

Cited by 4 publications

References 23 publications

Stage 2 hypertension in a child with a rapidly enlarging kidney: answer

Stage 2 hypertension in a child with a rapidly enlarging kidney: answer

Focal segmental glomerulosclerosis and nephrotic syndrome in a child with embryonal rhabdomyosarcoma

Stage 2 hypertension in a child with a rapidly enlarging kidney: question

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