Case Summary Patrick M. Yalung MD080070 I.

Salient Features Patient is a 10 year old male who came in due to headache and vomiting. Few hours PTC, patient developed headache that was graded 9/10 in intensity, was bilateral, frontal in location, and pressing in character. No aggravating factors were noted. Pain was partially relieved by 3 episodes of vomiting partially digested food. Vomiting was non-projectile. Vomitus was non-blood tinged, non-bilous. Headache was accompanied by photophobia. Patient had no blurring of vision, fever or urinary symptoms. Patient was given unrecalled dosage of paracetamol which provided no relief. Persistence of headache prompted consult. It was noted that patient had chest pain and tonsillitis 2 weeks PTC. Patient is conscious, coherent, not in CR distress. BP= 160/110 (>P99), HR= 84 (Normal), RR= 24 (tachypneic), T= 36.6oC (afebrile). The rest of the PE is essentially normalpink palpebral conjunctiva, anicteric sclera; moist oral and buccal mucosa; clear breath sounds; normal cardiac rate and rhythm; soft, non-tender abdomen; full, equal pulses; CRT<2; no edema; GCS= 15; oriented to 3 spheres; CNs intact; motor= 5/5 on all extremities; sensory= 100%; reflexes= +2 on all; no meningeal signs. II. Differential Diagnoses Considerations include space occupying mass in the brain that might be causing the headache and increased ICP causing the vomiting; migraine; urgency hypertension secondary to probable post-streptococcal GN. III. Working Diagnosis Urgency Hypertension probably secondary to post-streptococcal glomerulonephritis IV. Diagnostic Work-Up The following labs were requested: CBC was done to rule out infection; Serum electrolytes was requested to rule out electrolyte imbalance; BUN, Creatinine were requested to assess renal function; C3 was ordered to rule-out AGN; CXR and ECG were requested to rule out cardiac causes and since patient complained of chest pain 2 weeks PTC; CT to rule out masses that might have caused the symptoms; UA to check for proteinuria and hematuria. The above tests showed the following abnormal results: elevated WBC, predominantly segmenters; elevated serum creatinine; low C3, elevated uric acid, hematuria (+4) and proteinuria (+1). The following tests could also have been ordered: ASO titer to confirm streptococcal infection. V. Final Diagnosis Urgency Hypertension probably secondary to post-streptococcal glomerulonephritis VI. Discussion A. Etiology Acute poststreptococcal glomerulonephritis (APGN) follows infection of the throat (serotype 12) or skin (serotype 49) by certain "nephritogenic" strains of group A hemolytic streptococci.

Case Summary Patrick M. Yalung MD080070 B. Pathophysiology APGN is a classic example of the acute nephritic syndrome characterized by the sudden onset of gross hematuria, edema, hypertension, and renal insufficiency. It is the most common glomerular cause of gross hematuria among children in the country and is second to IgA nephropathy in the world. APGN is most common in children aged 5-12 yr. The typical patient develops an acute nephritic syndrome 1-2 weeks after an antecedent streptococcal pharyngitis or 3-6 weeks after a streptococcal pyoderma. The severity of renal involvement varies from asymptomatic microscopic hematuria with normal renal function to acute renal failure. Patient may also develop various degrees of edema, hypertension, and oliguria. Patient may also develop encephalopathy and/or heart failure owing to hypertension or hypervolemia. Encephalopathy may also result due to bacteremia. Edema results from salt and water retention. Nephrotic syndrome may develop in 10-20% of cases. Specific symptoms such as malaise, lethargy, abdominal or flank pain, and fever are common. The acute phase generally resolves within 6-8 weeks. Although urinary protein excretion and hypertension usually normalize by 4-6 weeks after onset, persistent microscopic hematuria may persist for 1-2 yr after the initial presentation. As in most forms of AGN, the kidneys appear symmetrically enlarged. On light microscopy, all glomeruli appear enlarged and relatively bloodless and show diffuse mesangial cell proliferation with an increase in mesangial matrix. PMNs are common in glomeruli during the early stage of the disease. Crescents and interstitial inflammation may be seen in severe cases. Immunofluorescence microscopy reveals lumpy-bumpy deposits of immunoglobulin and complement on the glomerular basement membrane and in the mesangium. On electron microscopy, electron-dense deposits are observed on the epithelial side of the GBM. Although morphologic studies and a depression in the serum C3 level strongly suggest that post-streptococcal glomerulonephritis is mediated by immune complexes, the precise mechanisms by which nephritogenic streptococci induce complex formation remain to be determined. C. Treatment Management is directed at treating the acute effects of renal insufficiency and hypertension. Sodium restriction, diuresis, and pharmacotherapy with calcium channel antagonists, vasodilators, or angiotensin-converting enzyme inhibitors are standard therapies used to treat hypertension. A 10-day course of systemic antibiotic therapy with penicillin is recommended to limit the spread of the nephritogenic organisms, although this does not affect the natural history of glomerulonephritis. D. Prevention Early systemic antibiotic therapy for streptococcal throat and skin infections does not eliminate the risk of glomerulonephritis. Family members of patient should be cultured for group A -hemolytic streptococci and treated if culture positive.

Case Summary Patrick M. Yalung MD080070 E. Prognosis Complete recovery occurs in more than 95% of children with acute poststreptococcal glomerulonephritis. Mortality in the acute stage can be avoided by appropriate management of acute renal failure, cardiac failure, and hypertension. Infrequently, the acute phase may be severe and lead to glomerular hyalinization and chronic renal insufficiency. Recurrences are extremely rare. Acute complications of this disease result primarily from hypertension and acute renal dysfunction. Hypertension is seen in 60% of patients and may be associated with hypertensive encephalopathy in 10% of cases. Other potential complications include heart failure, hyperkalemia, hyperphosphatemia, hypocalcemia, acidosis, seizures, and uremia. VII. References Nelsons Textbook of Pediatrics, 19th ed