This document summarizes various kidney diseases and disorders: 1) It describes different types of glomerulonephritis including acute glomerulonephritis caused by Streptococcus infection and rapidly progressive glomerulonephritis associated with immune disorders. 2) It also outlines Goodpasture's syndrome, Wegener's granulomatosis, Henoch-Schonlein purpura, IgA nephropathy, membranous glomerulonephritis, and membranoproliferative glomerulonephritis. 3) Additional sections cover chronic glomerulonephritis, nephrotic syndrome, minimal change disease, focal segmental glomer

2. What is human but an ingenious
machine designed to turn, with
“infinite artfulness, the red
wine of Shiraz into urine”?
Storyteller in Isak Dinesen’s Seven Gothic Tales

7. ACUTE GLOMERULONEPHRITIS
 Deposition of immune complexes
formed in conjunction with group A
Streptococcus infection
 Macroscopic hematuria, proteinuria rbc
and granular casts
 Antistreptolysin O titer and Anti-group A
streptococcal enzymes

8. RAPIDLY PROGRESSIVE (CRESCENTRIC)
GLOMERULONEPHRITIS
 Deposition of immune complexes from
systemic immune disorders on the
glomerular membrane (i.e. Systemic Lupus
Erythematosus)
 Macroscopic hematuria, proteinuria and
rbc casts
 BUN, Creatinine and Creatinine clearance
 Possible progression of ESRF

9. This immunofluorescence micrograph of a glomerulus demonstrates positivity
with antibody to fibrinogen. With a rapidly progressive GN, the glomerular
damage is so severe that fibrinogen leaks into Bowman's space, leading to
proliferation of the epithelial cells and formation of the bright crescent.

10. GOODPASTURE’S SYNDROME
 Cytotoxic antibody formed during viral
respiratory infection attach to glomerular
and alveolar basement membrane
 Hemoptysis and dyspnea followed by
hematuria, proteinuria and rbc casts
 Antiglomerular basement membrane
antibody

11. This immunofluorescence pattern shows positivity with antibody to IgG
and has a smooth, diffuse, linear pattern that is characteristic for
deposition of antiglomerular basement membrane antibody with
Goodpasture syndrome.

12. WEGENER’S GRANULOMATOSIS
 Antineutrophilic cytoplasmic antibody
binds to neutrophils
in vascular walls
 Pulmonary symptoms (hemoptysis)
followed by hematuria, protenuria and
rbc casts
 ANCA test
 Progress to ESRF

13. HENOCH-SCHONLEIN PURPURA
 Occurs in children after
viral respiratory infection
 Initial appearance of purpura followed by
blood in stool and sputum then renal
involvement
 Stool occult blood

14. IgA NEPHROPATHY/
Berger’s Disease
 Deposition of IgA on glomerular
membrane resulting from increased
levels of serum IgA
 Recurrent macroscopic hematuria
following mucosal infection or strenuous
exercise
 Slow progression to CGN

15. MEMBRANOUS
GLOMERULONEPHRITIS
 Most common cause of Nephrotic
Syndrome in Adult
 Thickening of glomerular basement
membrane from deposition of IgG
immune complexes
 Associated with SLE, Sjogrens
syndrome, secondary syphilis, Hep B
and malignancy
 ANA, HbS Ag and FTA-ABS

16. MEMBRANOPROLIFERATIVE
GLOMEROLUNEPHRITIS
 Cellular proliferation affecting the capillary
walls or glomerular basement membrane
 Double contour or “tram-track” appearance
 Subendothelial deposits of C3, IgG, C1, C4
 Hematuria and proteinuria
 Slow progression to nephrotic syndrome or
possible remission
 Serum complement level

17. Membranoproliferative
glomerulonephritis (MPGN).
-glomerulus has increased
overall cellularity
- Silver stain “tram-tracking”
characteristic

18. CHRONIC
GLOMERULONEPHRITIS
 Marked decreased in renal function due
to glomerular damage precipitated by
other renal disorders
 Hematuria, proteinuria, glucosuria, urin
e casts (cellular, granular, waxy and
broad)
 BUN, Creatinine, Creatinine
clearance, Electrolytes

19. NEPHROTIC SYNDROME
 Acute onset following systemic shock
 Gradual progression from other gromerular
disorder to renal failure
 Massive proteinuria
(>3.5), hypoalbuminemia, generalized
edema, hyperlipidemia & lipidosis
 Microscopic hematuria, renal tubular
cells, oval fat bodies and fat droplets, fatty
and waxy casts
 Serum albumin, cholesterol and
triglycerides

20. MINIMAL CHANGE DISEASE
(Lipid Nephrosis)
 NS in children after allergic reactions
and immunizations
 Heavy proteinuria, transient hematuria
and fat droplets
 Complete remission following
corticosteroid treatment
 Serum albumin, cholesterol and
triglycerides

21. Thickened Basement Membrane Effaced foot processes
Minimal change disease (MCD) characterized by effacement of the epithelial cell
(podocyte) foot processes and loss of the normal charge barrier

22. FOCAL SEGMENTAL
GLOMERULONEPHRITIS
 Disruption of podocytes in some areas
of glomeruli associated with
heroin, analgesic abuse and HIV
 May resemble nephrotic syndrome or
minimal change disease
 Drugs of abuse and HIV test

23. An area of collagenous sclerosis
runs across the middle of this
glomerulus
Trichrome stain of a
glomerulus in a patient with
focal segmental
glomerulosclerosis (FSGS)
demonstrates blue collagen
deposition.

24. ALPORT SYNDROME
 Inherited sex linked or autosomal disorder
 Males before age 6 during a respiratory
infection may exhibit macroscopic
hematuria and continue to exhibit
microscopic hematuria
 Abnormal vision and hearing may be
present

25. DIABETIC NEPHROPATHY
 a.k.a. Kimmelstiel-Wilson disease
 Deposition of glycosylated proteins due to
uncontrolled blood glucose level
 Early monitoring of px with
microalbuminuria is important
 Most common cause of End Stage Kidney
Disease.

27. ACUTE TUBULAR NECROSIS
 Damage to renal tubular cells caused by
ischemia or toxic agents
 Reversible renal dysfunction
 Microscopic
hematuria, proteinuria, RTE cells and
casts (hyaline, granular, broad and
waxy)
 Hemoglobin, hematocrit and cardiac
enzymes

28. HEREDITARY METABOLIC
TUBULAR DISORDERS

29. FANCONI’S SYNDROME
 Inherited or acquired through exposure
to toxic agents, outdated tetracycline or
complication of Multiple Myeloma.
 Generalized defect in renal tubular
reabsorption in proximal convoluted
tubules
 Glucosuria and possible cystine crystals
 Serum and urine electrolytes, amino
acid chromatography

30. NEPHROGENIC DIABETES
INSIPIDUS
 Inherited sex-linked recessive or
acquired from medication or as
complication of PCKD or sickle cell
anemia
 Inability of renal tubules to respond to
ADH causing polyuria
 Urine is pale yellow, and with low
specific gravity

31. RENAL GLYCOSURIA
 Generalized failure to reabsorb
substances from glomerular
filtrate, affecting the reabsorption of
glucose
 Increased urine glucose concentration
with normal blood glucose.

34. CYSTITIS
 Ascending bacterial infection of the
bladder
 Acute onset of urinary frequency and
burning resolved with antibiotics
 Leukocytoria, bacteruria, microscopic
hematuria, mild proteinuria and
increased pH
 Urine culture

35. ACUTE PYELONEPHRITIS
 Renal tubulointerstitial infection related
to interference of urine flow to the
bladder, urine reflux or untreated cystitis
 Acute onset of urinary frequency and
burning resolved with antibiotics
 Leukocytoria, bacteruria, Casts
(WBC, bacterial, granular, waxy and
broad) hematuria and proteinuria
 Urine and blood cultures

36. CHRONIC
PYELONEPHRITIS
 Recurrent renal tubulointerstitial infection
caused by structural abnormalities affecting
urine flow
 Diagnosed in children and requires
correction of structural defects
 Leukocytoria, bacteruria, Casts
(WBC, bacterial, granular, waxy and
broad) hematuria and proteinuria
 Urine and blood cultures, BUN, Creatinine
and Creatinine clearance

37. ACUTE
INTERSTITIAL NEPHRITIS
 Allergic inflammation of renal interstitium
in response to certain medications
 Acute onset of renal dysfunction
accompanied by skin rash
 Resolves with discontinuation of
medication and treatment with
corticosteroids
 Hematuria, proteinuria, leukocyturia and
WBC casts
 Urine eosinophils, BUN, creatinine and
creatinine clearance

38. VASCULAR DISORDER
 Renal ischemia and loss of functional
renal tissue
 Disorders that affect integrity of renal
blood vessels:
- Autoimmune disorders
- Vaculitis
- Diabetes mellitus

39. RENAL LITHIASIS
 May form in calyces and pelvis of KUB
 Renal colic or flank pain
 Vary from barely visible to
staghorn calculi
 75% compose of calcium oxalate
and phosphates
 Lithotripsy and surgery

40. RENAL FAILURE
 Exists in both acute and chronic forms
 Gradual progression from the original
disorder to end-stage renal disease
Renal insufficiency
Acute Renal Failure
Chronic Renal Failure

41. Acute Renal Failure
Prerenal: decreased blood pressure and
cardiac
output, hemorrhage, burns, surgery
and septicemia
Renal: Acute glomerulonephritis, Acute
tubular necrosis, Acute
pyelonephritis, Acute interstitial necrosis
Postrenal: Renal calculi, Tumors and
Crytallization of ingested substances
Chronic Renal Failure

42. Chronic Renal Failure
- marked decreased in GFR
- rising BUN and creatinine (AZOTEMIA)
- electrolyte imbalance
- Isothenuria, proteinuria, glycosuria
- Abundance of granular, wax and broad
casts
END-STAGE RENAL DISEASE

45. Thank You!