July 2008.indd Varied Presentations of Acute Glomerulonephritis in Children Single centre experience from a developing country *Kalpana Malla, Moinak S Sarma, Tejesh Malla, Anna Thaplial SULTAN QABOOS UNIVERSITY MEDICAL JOURNAL JULY 2008, VOLUME 8, ISSUE 2, P. 193-199 SULTAN QABOOS UNIVERSITY© SUBMITTED - 11TH SPETEMBER 2007 ACCEPTED - 21TH APRIL 2008 C L I N I C A L A N D B A S I C R E S E A R C H عند األطفال لَى احلاد الكُ بَيباتِ كُ اللْتِهابُ العروض اتلفة في دولة نامية جتربة مركز منفرد ثاباليل أنا مال، تيجيش سارما، مويناك مال، كالبانا اتلفة ــريرية الس العروض التعليمي في بخارى لتوثيق مانيبال ــفى مستش في أجريت ــتباقية التي االس ــة الدراس الهدف: هدفت هذه امللخص: واتبرية ــريرية الس ُتَثابِتَات الطريقة: امل الغربية. نيبال في املتوفرة البيولوجية ُتَثابِتَات امل مع ومقارنة ذلك ، األطفال عند احلاد لَى الكُ بَيباتِ كُ اللْتِهابُ بالتهاب 92 طفال ــخيص مت تش (2007-2000) ــنوات ــبع س العيانية واهرية. النتائج: خالل س وِيَّة مَ الدَ والبِيلَةٌ الوذمة من يعانون الذين لألطفال اللْتِهابُ اتلفة العروض على الضوء ــلطت س احلالية ــة اخلالصة: الدراس باألحداث. زاخرة واتبرية كانت ــريرية الس التحليالت . احلاد لَى الكُ بَيباتِ كُ النيبال. من الغربية في املنطقة الكالسيكية العروض من انتشارا أكثر منطية الال واملضاعفات العروض أن وبينت ، احلاد لَى الكُ بَيباتِ كُ نيبال. ، البولية ااري التهاب ، حاد ، لَى الكُ بَيباتِ كُ الْتِهابُ ، الكلمات: مرض الكلية مفتاح Department of Pediatrics, Manipal College of Medical Sciences, Pokhara, Nepal * To whom correspondence should be addressed. Email: kalpana17@hotmail.coms ABSTRACT: Objectives: The objective of this prospective study, carried out at Manipal Teaching Hospital, Pokhara, was to document the various clinical presentations of children with acute glomerulonephritis and compare them with the available biological param- eters in Western Nepal. Methods: Clinical and laboratory parameters of children with oedema and microscopic/macroscopic hae- maturia. Results: For seven years (2000-2007), 92 cases of children were clinically diagnosed with acute glomerulonephritis (AGN). Other clinical and laboratory anaylses were also eventful. Conclusion: The present study highlights the varied presentations of AGN, atypical presentations or complications of glomerulonephritis being more common than the classical presentation in the Western Region of Nepal. Key words: Renal disease; Glomerulonephritis, acute; Urinary tract infection; Nepal. GLOMERULONEPHRITIS (GN) IS THE TERM generally reserved for the variety of re-nal diseases in which inflammation of the glomerulus, manifested by proliferation of cellular ele- ments, is secondary to an immunologic mechanism.1 Most incidents of AGN appear to be associated with a postinfectious state with known aetiological agents like bacteria, parasite, virus. Amongst the GN second- ary to bacterial infections, post-streptococcal GN is the most frequent and usually presents with typical clinical findings;2 however, the scenario in this study was different. Out of 92 cases of acute glomerulone- phritis, only 33 cases presented with typical clinical features of GN; the remaining 59 had atypical clinical presentations. Atypical postinfectious glomerulone- phritis (PIGN) may mimic a great variety of glomeru- lar diseases.3, 4 M E T H O D S This prospective study was conducted between Sep- tember 2000 and March 2007 at the Department of Pediatrics, Manipal Teaching Hospital, Pokhara, Ne- pal. The case collection was from September 2000 to February 2005 and follow-up was continued until March 2007. Ninety-two children of all age groups presenting either with oedema (facial puffiness and/or K A L PA N A M A L L A , M O I N A K S S A R M A , TE J E S H M A L L A A N D A N N A TH A P L I A L 194 pedal oedema) and haematuria (microscopic or frank and/or cola coloured urine) were considered for this study. Borderline cases, those with urinary stones and with hypercholesterolemia suggestive of nephrotic syndrome, (4+ protenuria with high cholesterol level requiring treatment with prednisolone) were excluded from the study. Both outpatients as well as hospital- ized patients were enrolled for the study. Consent of the patients was taken and the parents or guardians received information about the study and follow-ups. A detailed history was taken and a clinical examina- tion performed, followed by relevant available inves- tigations. The investigations included urine routine and microscopic examination, urine culture and sen- sitivity, renal function tests, antistreptolysin O (ASO) titres and ultrasound of the abdomen. Facilities for doing serum complement levels, electron microscopy and immunofluroscence studies for renal biopsy were not available in this centre. These cases were followed up for two years. R E S U L T S Of the 92 children, 57 (61.95%) were male and 35 (38.05%) were female. All were diagnosed to have acute glomerulonephritis (AGN). The male: female ratio was 1.6:1. Eighty-eight children (95.7%) were above 5 years (school going age group); only four (4.3%) of the chil- dren were under 5 years (preschool age group) [Table 1]. The classical presentation of AGN was seen only in 33 (35.9%) cases, while 59 (64.1%) presented with atypical findings or complications [Figure 1]. The pat- tern of atypical presentations/complications were hy- pertensive encephalopathy (n = 11, 18.6%); nephrotic onset (n = 10, 16.9%); urinary tract infection (UTI) (n = 10, 16.9%); joint pains and rash (n = 2, 3.3%); heart failure (HF) (n = 6, 10.1%); combined HF and UTI (n = 3, 5.1%); rapid deterioration or progression (n = 5, 8.5%); acute renal failure (n = 4, 6.7 %); combined car- diac and renal failure (n = 1, 1.69 %), associated with rheumatic fever (n = 3, 5.1%); epistaxis (n = 2, 3.3%); malena (n = 1, 1.69%); associated with enteric fever and UTI (n = 1, 1.69 %) [Table 2]. Clinically, all (100%) children had facial puffiness and/or pedal oedema and macroscopic haematuria (frank and/or cola coloured urine). Other main clini- cal features were hypertension (n = 80, 86.9%), fever (n = 60, 65.2%), headache (n = 58, 63.0%) and oliguria (n = 50, 54.3%) followed by pyodermas, vomiting, burn- ing micturition, painful abdomen, sore throat, altered sensorium, convulsions and shortness of breath. Some rare clinical features were also noted cough (n = 14, 15.2%), systolic murmur (n = 7, 7.6%), joint pains and rash (n = 2, 2.1 %), hepatomegaly (n = 3, 3.2 %), diar- rhoea (n = 3, 3.2 %), epistaxis (n = 2, 2.1 %), malena (n = 1, 1.0 %) [Table 3]. Table 4 shows the results of the investigations into urea, creatinine and albumin levels in these patients. ASO titres were found to be positive in only 50% of Sex Age <1yr >1-5yr >5-10yr >10yr Male = 57 (61.95 %) Female = 35 (38.04%) 0 0 3 1 21 12 33 22 Acute Glomerulonephritis (AGN) (n = 92) Total 0 4 33 55 92 Table 1: Age and Sex distribution of patients at presentation Figure 1: Clinical Presentation VA R I E D P R E S E N TAT I O N S O F A C U T E G L O M E R U L O N E P H R I T I S I N C H I L D R E N 195 the cases. An ultrasonography (USG) of the kidney, ureters and bladder revealed Grade I renal parenchy- mal changes (RPC) in 48%; Grade II RPC, mild renal dysfunction (MRD) in 24%; Grade III RPC in 6.5% and normal in 22% cases [Figure 2]. All the three renal bi- opsies showed cresentric glomerulonephritis. D I S C U S S I O N The global burden of severe Group A streptococcal disease is concentrated largely in developing countries including Nepal. Group A streptococcal diseases are more common in children than in adults with diseases ranging from pharyngitis and impetigo to invasive in- fections and the post-streptococcal sequelae: acute rheumatic fever and acute post-streptococcal glomerulonephritis.3 Acute post-streptococcal glomerulonephritis is the commonest cause of AGN in this country which usually exhibits milder symp- toms or signs like haematuria, mild oedema, oliguria and hypertension which has a simple clinical course and an excellent prognosis. On the other hand, atypi- cal presentations may mimic a great variety of glomer- ular disease, have a worse prognosis and need better diagnosis and care. Glomerular disease with atypical presentations will include mild mesangial and/or en- docapillary glomerulonephritis (GN); focal segmental glomerulosclerosis (FSGS) with diffuse IgM mesangial deposits; rapidly progressive or crescentic GN with C3 hump-like deposits or with microabscesses; focal me- sangiocapillary GN superimposed on endocapillary pattern; membranous GN with diffuse exudative changes and postinfectious glomerulonephritis with anti–glomerular basement membrane (anti-GBM) linear deposits.4 Some other study states that mesang- ial proliferative GN is the commonest histopathologi- cal lesion forming 66% of all primary GN. Minimal le- sion, focal global sclerosis and focal segmental glomerulosclerosis accounted for 7% each. Membra- nous GN was uncommon (3%), while mesangiocapil- lary GN, diffuse endocapillary GN and crescentic GN were even rarer.5 In this study, we tried to ascertain age incidence, sex ratio, common clinical presentations and available biochemical parameters of primary glomerulonephritis. Out of 92 children, there were 59 atypical findings of AGN. Those with positive ASO titres were treated as poststreptococcal glomerulone- phritis cases. The others were given the benefit of the doubt and treated for the same. Lack of facilities for investigations and financial constraints in a develop- ing country did not permit us to proceed with further workups. Hence the confirmatory diagnosis could not be made in these cases. Like other studies, this study also showed a preponderance of males (61.95%) as AGN cases (n = 59) Number Percentage AGN with hypertensive encephalopathy 11 18.6% AGN with nephrotic picture 10 16.9 % AGN with urinary tract infection (UTI) 10 16.9 % AGN with heart failure 6 10 .1% AGN with rapid progressive GN 5 8.5% AGN with acute renal failure 4 6.7 % AGN with rheumatic fever 3 5 % AGN with heart failure + UTI 3 5 % AGN with joint pains and rash 2 3.3 % AGN with epistaxis 2 3.3 % AGN with malena 1 1.69% AGN with heart failure and acute renal failure 1 1.69 % AGN with enteric fever and urinary tract infection 1 1.69 % Total 59 100% Table 2: Pattern of atypical presentations/complica- tions of acute glomerulonephritis (AGN) Table 3: Signs and Symptoms of patients at presen- tation Signs and symptoms Number (n=92) percentage Hypertension 80 86.9% Fever 60 65.2% Headache 58 63% Oliguria 50 54.3% Pyoderma 42 45.6 % Vomiting 33 35.8 % Burning urine 32 34.7 % Pain abdomen 31 33.6 % Sore throat 28 30.4 % Altered sensorium 21 22.8 % Convulsions 21 22.8 % Shortness of breath 18 19.5% Cough 14 15.2 % Systolic murmur 7 7.6 % Hepatomegaly 3 3.2 % Diarrhoea 3 3.2 % Joint pain with rash 2 2.1 % Epistaxis 2 2.1 % Malena 1 1.0 % K A L PA N A M A L L A , M O I N A K S S A R M A , TE J E S H M A L L A A N D A N N A TH A P L I A L 196 compared to females (38.05%) with the ratio 1.6:1. The reasons for this male predominance are not known.1 As in other studies,6 most children were above 10 yrs (57.9%). Hypertensive encephalopathy was found in 18.6%, a much higher percentage compared to 5% & 4.3 % in other studies. 7, 5 In these patients, hyperten- sion is usually difficult to control and accompanied by signs of central nervous system dysfunction such as headaches, vomiting, depressed sensorium, confusion, visual disturbances, aphasia, memory loss, coma, and convulsions. All these features were also noted in our study. Twelve of the cases, which presented as neph- rotic onset, had anasarca with proteinuria >40 mg/ m2/hr. All of them (100%) had haematuria and hyper- tension; their features resolved with symptomatic treatment and did not require steroids. The incidence of nephrotic features was higher in other studies, 61.7%, 66%, 29% and 34.48% respectively as compared to ours which was only 13%. 5, 8-10 Seventeen percent had associated UTI which is quite frequently seen. AGN complicated by UTI was also observed in 20% cases in a study in Nigeria.11 Rapidly progressive glomerulonephritis (RPGN) is a disease of the kidney that results in a rapid decrease in the glomerular filtra- tion rate of at least 50% over a short period, from a few days to 3 months and is irreversible.12 This was ob- served in 8.5 % in our study. The frequency is estimat- ed at 1-2 cases per 100,000 persons internationally. The main pathologic finding is fibrinoid necrosis (>90% of biopsy specimens); extensive crescent forma- tion is present in at least 50% of glomeruli.12 As biopsy was not done in our cases we could not confirm the cases by pathological findings, hence the observed fre- quency was higher. Heart failure (HF) and acute renal failure (ARF) were the sole systemic complications in 7/29 and 2/29 in AGN patients respectively, noted by Olowa WA in Nigeria.10 Heart failure was seen in 3% cases in another study, 13 whereas in our study 10% presented with shortness of breath, cough, hepatome- galy. Acute renal failure is defined as abrupt or rapid decline in renal filtration function. The condition is of- ten transient and usually completely reversible.14Acute renal failure was present in 56 (76%) in one study and dialysis required in 14, but this presentation was much less in our study and only 4 required dialysis.9 We also observed some rare features like rheumatic fever (5%), epistaxis in 2 patients, melena in one. Literature on these presentations was not available. A few double systemic complications were also noted: AGN with enteric fever with UTI (1.69%), AGN with HF and ARF (1.69%).Three patients had double systemic com- plications in another study: one with hypertensive en- cephalopathy (HTE) with HF, and two with acute renal failure (ARF) with HF.10 The development of clinical nephritis (i.e. haematuria and/or oedema) either dur- ing or within 2-5 days after the onset of a respiratory tract infection is atypical and suggests the possibility of some other form of GN.15 In our study, nephritis de- veloped following respiratory infection in 15% cases. Hypertension was the commonest mode of presenta- tion (87%) in a study by Corpa, Soares V. The preva- lence of arterial hypertension was 62.7%16 and it was 50% and 86.7% respectively in another study. 17, 8 The pathogenesis of the hypertension is unknown; howev- Parameters Number Percentage Urea : Normal range 0.535-14.28mmol/L (15-40mg/dl) <14.28mmol/L (< 40mg/dl) 14.63-17.85mmol/L (41-50mg/dl) 18.20-35.70mmol/L (51-100mg/dl) >35.70mmol/L (>100mg/dl) 40 22 20 9 43.5% 24% 22% 10% Creatinine: Normal range 53.04-132.6µmol/L (0.6-1.5mg/dl) <132.6µmol/L (<1.5mg/dl) 141.44-142µmol/L (1.6-5mg/dl) >142µmol/L (5 mg/dl) 54 23 15 59% 25% 16% Albumin: Normal range 3.5-5gm/dl <25gm/L (2.5 g /dl) 26-30gm/L (2.6 -3.0g/dl) 31-35gm/L (3.1 - 3.5 g/dl) >35gm/L (3.5g/dl) 16 38 18 20 17.4% 41% 19.6% 22% Table 4: Biochemical parameters of the patients VA R I E D P R E S E N TAT I O N S O F A C U T E G L O M E R U L O N E P H R I T I S I N C H I L D R E N 197 er, it is probably multifactorial and related only in part to extracellular fluid (ECF) volume expansion. Haema- turia and protenuria was present in 41% in one study5 and in 48.8% in another study.8 According to some in- vestigators, oedema is found in approximately 85% of patients.15 Oedema usually appears abruptly and the degree of oedema varies markedly and depends on a number of factors, including the severity of glomeru- lar involvement, the fluid intake, and the degree of hy- poalbuminaemia. In our study also the degree of oede- ma was variable. Gross haematuria occurs at onset in 30-50% of children with poststreptococcal glomeru- lonephritis (PSGN) who require hospitalisation.18 The cardinal features are associated with various degrees of malaise, lethargy, anorexia, fever, abdominal pain and headache. Observant parents may also note oligu- ria. All these features were observed in this study. Al- most characteristic by their absence are arthralgia, arthritis, carditis, hepatic involvement, and gastroin- testinal bleeding, 19, 17 but in this study these findings were also noted. Systolic murmur was observed in 7.6% of the cases, hepatomegaly in 3%, diarrhoea in 3% and joint pain with rash in 2%. In this study, pyoderma and sore throat were the preceding cause of GN in 46% and 30 % of cases respectively. This indicates the pos- sibility of post streptococcal origin; however, in the remaining 24% cases there was no preceding pyoder- ma or sore throat. Other postinfectious causes that have been reported are: Streptococcus pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis, Rickettsia rickettsiae, Mycoplasma species, Meningo- coccus species, Leptospira species. Also, viral illnesses have preceded the onset of typical AGN; among the most common are the varicella zoster virus, cytomeg- alovirus, and the Epstein-Barr virus.20 In the analysis of laboratory parameters, it was noted that impair- ment of urea was seen in 56% and impairment of cre- atinine in 41%. Renal impairment observed in other studies was 33.3%8 and 5.5% respectively. 8, 21,19 Low al- bumin levels of >35gm/L were observed in 78% of cases (25gm/L in 17.4%; 26-30gm/L in 41%; 31-35gm/ L in 19.6%) and normal levels of >35gm/L in 22%. In the majority (60.6%) of cases it was between 2.6 - 3.5 g/dl. The reason why many patients had albumin levels slightly on the low side can be explained by the fact that these children were malnourished, which is again a common problem of this country. A rise in the titer of ASO is observed in only 50% of patients.22, 20 In our study too, ASO was positive in 50% of cases. Ultra- sound of the kidney, ureters and bladder was normal in 22% cases. Forty-eight percent of patients with RPC had RPC Grade I (RPC), 24% had Grade II, and 6.5% had Grade III. RPC Grade I is echogenicity of kidney the same as the liver, RPC Grade II is echogenicity of the kidney more than the liver. RPC Grade III means that renal fat sinus and renal parenchyma cannot be differentiated with accentuated/ATT - corticomedul- lary differentiation.23, 21 The follow-up of this study was not good as just over half the patients (52.5%) did not return for follow- up. Maybe the referral to a higher level centre was the reason for this. Among those who came for follow-up, the ones with classical presentation AGN had com- plete resolution of the disease. Complete resolution was also observed in 42.85% cases that had atypical or complicated presentations. This means many may still have fallen into postinfectious forms, which are very common in our environment. Of these, 32.14% Classical presentation (n = 33) Atypical or complicated presentation (n = 59) Follow-up Yes No 33 (100%) 0 (0%) n = 33 28 (30.4%) 31 (52.5%) n = 59 - Complete resolution - With impaired renal function - End stage renal disease on haemodialysis at higher centre - Mortality 33 (100%) 0 (0%) 0 (0%) 0 (0%) n = 33 12 (42.85%) 9 (32.14%) 5 (17.85%) 2 (7%) n = 28 Table 5: Follow-up of patients K A L PA N A M A L L A , M O I N A K S S A R M A , TE J E S H M A L L A A N D A N N A TH A P L I A L 198 had impaired renal function and 17.85% had gone into end stage renal disease and were on haemodialysis at a higher level centre. There was 7% mortality [Table 5]. The enlisted cases were provisionally assumed to be of poststreptococcal origin and were treated likewise since PSGN is the commonest cause in a developing country like ours. However, these cases, especially the ones which were ASO negative, needed better diag- nostic and confirmatory support such as complement C3, C4 levels and immunofluorescence for the biopsy specimens. These investigations were unfortunately unavailable at our setup and elsewhere in the city. Many investigations were also limited due to financial constraints of the patients. As optimum workup was required, we referred many of the cases to higher level centres. Some of these cases were subsequently lost to follow-up. C O N C L U S I O N We conclude that AGN is common in children of the Western region of Nepal and that an unusual atypi- cal presentation is frequent. Better outcomes can be achieved with more detailed laboratory and diagnos- tic methods which are limited at present. Renal biopsy in these cases is mandatory and helpful, especially in allowing rational use of corticosteroids and other im- munosuppressive drugs. Financial constraints are a major contributing factor in a developing country like Nepal. Nevertheless as PSGN is the commonest cause of GN in our country, it is justified to give the benefit of treatment to these patients before considering other causes. Symptomatic treatments and careful support- ive care will allow the majority of children to recover from post streptococcal AGN. A C K N OW L E D GE ME N TS The authors wish to thank all the patients and their parents for their co-operation. R E F E R E N C E S 1. Brouhard BH, Travis LB. Acute postinfectious glomeru- lonephritis. In: Edelman CM (Jnr), ed. Pediatric Kidney Disease. Boston: Little, Brown and Co, 1992. p. 1169- 1221. 2. Barbiano Di Belgiojoso G, Genderini A, Ferrario F. Post-infectious glomerulonephritis. G Ital Nefrol 2003; 20:184-99. 3. Steer AC, Danchin MH, Carapetis JR. Group A strep- tococcal infections in children. J Paediatr Child Health 2007; 43:203-213. 4. Sotsiou F, Dimitriadis G, Liapis H. Diagnostic dilemmas in atypical postinfectious glomerulonephritis. Semin Diagn Pathol 2002; 19:146-159. 5. Woo KT, Chiang GS, Edmondson RP, Wu AY, Lee EJ, Pwee HS, Lim CH. Glomerulonephritis in Singapore: an overview. Ann Acad Med Singapore 1986; 15:20-31. 6. Ali MS, Rahman S, Siddiqui NI, Talukder SI, Uddin MM, Sofiullah M, et al. Studies on clinical pattern of glomerulonephritis. Mymensingh Med J 2004; 13:33- 35. 7. Hoyer JR, Michael AF, Fish AJ, Good RA. Acute post- streptococcal glomerulonephritis presenting as hyper- tensive encephalopathy with minimal urinary abnor- malities. Pediatrics 1967; 39:412-417. 8. Mitwalli AH, Al Wakeel JS, Al Mohaya SS, Malik HG, Abu-Aisha H, Hassan OS, et al. Pattern of glomerular disease in Saudi Arabia . Am J Kidney Dis 1996; 27:797- 802. 9. Montseny JJ Meyrier A, Kleinknecht D, Callard P. The current spectrum of infectious glomerulonephritis. Ex- perience with 76 patients and review of the literature. Medicine (Baltimore),1995; 74:63-73. 10. Olowu WA. Systemic complications of acute glomeru- lonephritis in Nigerian children. Niger Postgrad Med J 2002; 9:83-87. 11. Michael IO, Gabriel OE Pattern of renal diseases in chil- dren in Midwestern zone of Nigeria. Saudi J Kidney Dis Transpl 2003; 14:539-544. 12. Andrassy K, Kuster S, Waldherr R, Ritz E. Rapidly pro- gressive glomerulonephritis: analysis of prevalence and clinical course. Nephron 1991; 59:206-212. 13 Lagunju IA, Omokhodion SI Childhood heart failure in Ibadan. West Afr J Med 2003; 22:42-45. 14. Agraharkar M, Safirstein RL. Pathophysiology of acute Figure 2: Results of ultrasonogram of kidney ure- ters and bladder region VA R I E D P R E S E N TAT I O N S O F A C U T E G L O M E R U L O N E P H R I T I S I N C H I L D R E N 199 renal failure. In: Greenberg A, Coffman T, eds. Primer on Kidney Diseases. 3rd ed. San Diego, Calif: Academic Press, 2001. p. 243-286. 15. Simckes AM, Spitzer A. Poststreptococcal acute glomerulonephritis. Pediatr Rev 1995; 16:278-279. 16. Corpa MV, Soares V. Systemic hypertension in patients with glomerulonephritis. Ren Fail 2002; 24:347-352. 17. Vujić D, Djukanović Lj, Petrović M, Radmilović A. Ar- terial hypertension in patients with primary glomeru- lonephritis. Srp Arh Celok Lek 1993; 121:130-132. 18. Dodge WF, Spargo BH, Travis LB, Srivastava RN, Carvajal HF, DeBeukelaer MM, et al. Poststreptococcal glomerulonephritis. A prospective study in children. N Engl J Med 1972; 286: 273-278. 19. Hricik DE, Chung-Park M, Sedor JR. Glomerulonephri- tis. N Engl J Med 1998; 339:888-899. 20. Travis LB: Acute postinfectious glomerulonephritis. In: Rudolph AM, Hoffman JI, Rudolph CD, eds. Rudolph’s Pediatrics. Stamford, CT: Appleton & Lange, 1996. p. 1356-1358. 21. Herthelius M, Berg U. Renal function during and after childhood acute poststreptococcal glomerulonephritis. Pediatr Nephrol 1999; 13:907-911. 22. Roy S 3rd, Stapleton FB: Changing perspectives in chil- dren hospitalized with poststreptococcal acute glomer- ulonephritis. Pediatr Nephrol 1990; 4:585-588. 23. Le Quesne GW. Assessment of glomerulonephritis in children by ultrasound. In: White D, Lyons EA, eds. Ul- trasound in Medicine, Vol. l4. New York: Plenum, 1978. p. 205-207.