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NEPHROLOGY DISORDERS

NEPHROLOGY DISORDERS. Tao Yuhong hxtyh@sina.com. Primary glomerular diseases. glomerulonephritis acute glomerulonephritis , AGN rapidly progressive glomerulonephritis , RPGN persistent glomerulonephritis chronic glomerulonephritis nephrotic syndrome, NS simple type NS)

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NEPHROLOGY DISORDERS

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  1. NEPHROLOGY DISORDERS Tao Yuhong hxtyh@sina.com

  2. Primary glomerular diseases • glomerulonephritis • acute glomerulonephritis, AGN • rapidly progressive glomerulonephritis, RPGN • persistent glomerulonephritis • chronic glomerulonephritis • nephrotic syndrome, NS • simple type NS) • nephritic type NS) • isolated hematuria or proteinuria • isolated hematuria • isolated proteinuria

  3. Acute glomerulonephrits

  4. Purpose and requirement • To understand the etiology, pathogenesis and pathology • To master the clinical manifestations (common case, severe case and atypical case), diagnosis and treatment • To understand the differential diagnosis and prognosis

  5. Definition • inflammation of the glomeruli • sudden appearance of hematuria, proteinuria，edema, and hypertension with or without oliguria • postinfectiousglomerulonephritis and immune mediated glomerulonephritis • acute poststreptococcalglomerulonephritis • follow streptococcal infections

  6. Age • typically affects children aged 5-15 years • 5% are younger than 2 years and 10% are older than 40 years.

  7. 1.Etiology • -hemolytic streptococcus, group A • antigen • components of cytoplasm & membrane • frequently CIC, sometimes ‘planted antigen’ • Others • other bacteria • viruses • parasites

  8. 1.Etiology • nephritogenic streptococci strains • pyoderma M types 47, 49, 55, 2, 60, and 57 • throat infection(pharyngitis) M types 1, 2, 4, 3, 25, 49, and 12.

  9. 2. Pathology Gross examination Swollen with scattered petechia

  10. Normal glomerulus Post-streptococcal glomerulonephritis • enlarged glomeruli • relatively bloodless • diffuse mesangial cell proliferation • increase in mesangial matrix.

  11. Pathology • Neutrophils infiltration WBC WBC WBC magnification ×1000, H&E stain , marked influx of polymorphonuclear leukocytes(arrows)

  12. Immunofluorescence Granular deposits lumpy - bumpy deposits of immunoglobulin and complement on the glomerular basement membranes and in the mesangium

  13. Subepithelial “lumps” immune complexes deposition Electron microscopy

  14. 3.Pathophysiology beta hemolytic streptococci （Ag） Form CIC or IC Glomerular local inflammation GBM damage Endocapillary proliferation GRF↓ Hematuria and proteinuria Water and salt rotention oilguria severe congestion of circulationor 和hypertensive encephalopathy Edema Extra celluar fluid volume ↑ hypertension

  15. 4.Clinical manifestation • Atypical patients • Asymptomatic( occasionally hematuria with/without proteinuria • Nephrotic syndrome • extrarenal form • Typical patients • Acute nephritic syndrome • Severe patients • severe congestion of circulation • Hypertensive encephalopathy • Acute renal failure

  16. 4.1 TypicalClinical features ---- Acute nephritic syndrome • The most frequent presentation • edema • hematuria • hypertension • with or without oliguria. • Approximately 95% of clinical cases have at least 2 manifestations • 40% have the full-blown acute nephritic syndrome.

  17. TypicalClinical features --- Preceding streptococcal infection Tonsillitis otitis media cervical adenitis impetigo

  18. TypicalClinical features--- latent period • between infection and the onset of acute glomerulonephritis. 1-2 weeks after a throat infection 3-6 weeks after a skin infection. • at the same time : more likely to be IgA nephropathy

  19. TypicalClinical features---hematuria（血尿） • May be microscopic and not identified by the patient, in more than two thirds of cases • May be macroscopic and lead to dark brown or tea-, or cola-colored urine • This is often the first clinical symptom. • caused by hemolysis of red blood cells that have penetrated the glomerular basement membrane and have passed into the tubular system.

  20. TypicalClinical features ---Edema • result of salt and water retention • acute onset • mild to modest severity • pitting edema • starts in the eye lids and face then the lower and upper limbs then generalized (Hydrocele, ascites. Pericardial and pleural effusion.) • may be migratory: appear in eyelid in the morning, disappear in the afternoon and reappear around the ankle in the ambulant patients by the end of the day

  21. TypicalClinical features---oliguria age normaloliguriaanuria infant 400-500 <200 toddler 500-600 <200 <30-50 preschool 600-800 <300 school 800-1400 <400 • present in 10-50% of cases • Anuria（无尿） : crescenticglomerulonephritis(新月体肾炎） • often transient, with diuresis occurring within 1-2 weeks

  22. TypicalClinical features --- Hypertension • occurs in 60-80% of cases • 50% of cases, hypertension can be severe; • often transient:with normalization of blood pressure upon restoration of the glomerular filtration rate, loss of edema, and normalization of plasma volume. • hypertension persists: more indicative of the progression to a more chronic stage or that the disease is not poststreptococcalglomerulonephritis. BP（mmHg） preschool >120/80 school >130/90

  23. TypicalClinical features --- Hypertension(高血压） • the result of excessive salt and water retention. • Hypertensive encephalopathy occurs in no more than 5-10% of patients. BP（mmHg） preschool >120/80 school >130/90

  24. Severe case-----severe congestion of circulation • 40% of elderly patients with APSGN. • an increase in blood volume secondary to retention of sodium and water not due to hypertension or myocarditis

  25. Severe case-----severe congestion of circulation • appear suddenly or the first manifestation of the disease Paroxysmal or persistent dispnea orthopnea apical gallop rhythm cardiac enlargement venous engorgement enlarged liver pulmonary edema

  26. Severe case-----Hypertensive encephalopathy • not common • children more frequently than adults. • not always attributable to severe hypertension • be the result of CNS vasculitis

  27. Severe case-----Hypertensive encephalopathy • Headache • Vomiting • irritability or apathy • convulsions • transitory paralyses • coma • temporary complete blindness

  28. Severe case -----Acute renal failure • less common • marked oliguria or anuria.

  29. 5.Laboratory findings • Urinalysis • Blood analysis • CBC ,ESR,renal function • C3 • ASO • IgA • ANA,ds-DNA • ANCA • EBV,HBV,HCV • Electrocardiogram • Chest X film • Ultrasound • Renal biopsy

  30. 5.Laboratory findings ----Urinalysis • Hematuria and proteinuria are present in all cases • Urine sediment has red blood cells, red blood cell casts, white blood cells, granular casts, and, rarely, white blood cell casts

  31. 5.Laboratory findings ----Urinalysis • Hematuria • Dysmorphic red blood cells indicative of glomerularhematuria • detected by performing phase-contrast microscopy. • usually resolves within 3-6 months • may persist as long as 18 months

  32. Laboratory findings ----Urinalysis Proteinuria • may be mild or severe • A mild increase in urinary protein excretion • present in 15% at 3 years and 2% at 10 years. • nephrotic-range proteinuria • Approximately 5-10% have. • in the acute phase or persistent heavy proteinuria • worse prognosis. • usually disappears in 6 months.

  33. 5.Laboratory findings ----Urinalysis (尿液分析） (3)Urine sediment • red blood cells, red blood cell casts • white blood cells, rarely, white blood cell casts • granular casts

  34. Laboratory findings ----- Elevated BUN and creatinine values • The elevations are usually transient. • failure to normalize within several weeks or months • not a true APSGN • suggests an alternative diagnosis. • rapid deterioration and incomplete recovery of renal function • have the crescentic form of glomerulonephritis have.

  35. Laboratory findings ----- Evidence of preceding streptococcal infection • Throat or skin culture • The antistreptolysin (ASO) • positive in more than 95% of patients with pharyngitis • 80% of patients with skin infections. • In general, the antibody titers are elevated at 1 week, peak at 1 month, and fall toward preinfection levels after several months.

  36. Laboratory findings----- estimation of complement components • Marked depression of serum C3. • indicative of an antigen-antibody interaction • the activation of the alternative pathway complement system • complement levels typically return to normal within 8 weeks • The level of reduction of serum complement levels does not have any prognostic significance.

  37. Laboratory findings----- estimation of complement components • Occasionally, low complement levels persist for 3 months. • Prolonged hypocomplementemia suggests an alternative diagnosis. • such as MPGN, endocarditis, occult sepsis, SLE, or congenital chronic state of complement deficiency

  38. Laboratory findings----- Imaging Studies • Chest radiographs findings of congestive heart failure. • Renal ultrasound images usually reveal normal-sized kidneys bilaterally.

  39. Laboratory findings----- Indication of renal biopsy • Atypical features in the early phase : • Absence of the latent period between streptococcal infection and acute glomerulonephritis • Anuria • Rapidly deteriorating renal function • Normal serum complement levels • No rise in antistreptococcal antibodies • Extrarenal manifestations of systemic disease • No improvement or continued decrease in the glomerular filtration rate at 2 weeks • Persistence of hypertension beyond 2 weeks

  40. Laboratory findings----- Indication of renal biopsy • Atypical features in the recovery phase: • Failure of glomerular filtration rate to normalize by 4 weeks • Persistent hypocomplementemia beyond 6 weeks • Persistent microscopic hematuria beyond 18 months • Persistent proteinuria beyond 6 months

  41. 6.Diagnosis(诊断) • Recent infection • latent period • Acute nephritic syndrome • acute onset • hematuria, frequently edema ,oliguria and hypertension • ASO , C3  —— dynamic change • Self-limitation

  42. 7.Differential diagnosis • GN secondary to infection of other pathogens • other bacteria, viruses (EB, influenza) • Climax of infection or within 5 days • Mild abnormal of urine examination • Hypertension and edema are unusual • Normal blood complement level

  43. 7.Differential diagnosis • IgA nephropathy • MPGN • acute crescentic glomerulonephritis • rapidly progressive GN • CGN • systemic diseases lupus nephritis, Schönlein-Henoch purpura

  44. 8.Treatment • usually supportive , directed toward the potential complications • Rest and salt restriction • Antibiotics to obliterate the streptococci • Symptomatic treatment：diuretic, antihypertensive drugs • Therapy for severe forms

  45. Treatment---Bed rest • Restricting physical activity • appropriate in the first few days of the illness • clinical manifestations of active disease, such as edema, hypertension, or gross hematuria • not necessary once the patient feels well.

  46. Treatment--- Diet • Restrictive intake of • NaCl • if moderate to severe edema or hypertension • Water • if decreased urine volume • Protein • Renal failure, but not dialysis yet

  47. Treatment --- Antibiotics(抗生素) • Object • Patients • high-risk individuals, including close contacts and family members • During epidemics, • Aim • prevent nephritis in carriers • helps prevent the spread of nephritogenic strains to others • Usage • Penicillin for 7-10 d • erythromycin for patients allergic to penicillin.

  48. Treatment ---Mild-to-moderate hypertension • does not warrant emergency management • most effectively with bedrest, fluid restriction • loop diuretics, such as furosemide (1-2 mg/kg/d oral [PO], administered 1-2 times daily • resistant to treatment, either hydralazineor nifedipineis indicated • ACE inhibitors are effective • have the potential to produce hyperkalemia • usually are not first-line drugs

  49. Treatment ---Severe hypertension • nitroprusside 0.5-2 mcg/kg/min ,IV • with severe hypertension • refractory to the previous agents • furosemide at doses of 2 mg/kg ,IV

  50. Treatment ---Edema and circulatory congestion • Restriction of fluids • the best treatment • Loop diuretics (furosemide) • furosemide parenterally (2 mg/kg) • marked congestion • Phlebotomy, rotating tourniquets, dialysis, or digitalization • rarely necessary

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