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1

Renal involvement usually follows a protracted course with periods of remissions and exacerbations (On & Off) immunosuppressive therapy

Lupus nephritis

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* In situ Immune Complex (Ag-Ab) formation

Fixed antigens ( intrinsic)/ anti GBM nephritis) Planted antigens (exogenous/ endogenous)

2

*Conditions associated with IgA nephropathy

Hepatic cirrhosis - Gluten enteropathy - HIV infection - Minimal change disease -Others: membranous, Wegener’s, Ankylosing spondylitis, small cell Ca

2

*75% of all bladder tumor

Urothelial carcinoma

Papillary carcinoma

2

-Dysuria, frequency, urgency -Low back/ pelvic or genital pain -Fever, Chills & leukocytosis -Loss of sex drive,

- painful erections / ejaculation *DRE: enlarged tender prostate

Prostatitis

3

1-Hematuria or proteinuria discovered on urinalysis 2-Acute nephritic syndrome with hematuria HTN and edema 3-Recurrent episodes of gross hematuria 4-Insidious onset of edema and nephrotic syndrome - Most progress to ESRD within 10-15 yearsa

Type II Membranoproliferative glomerulonephritis

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1-Renal ( primary kidney diseases)

Congenital - Acquired (glomerular / tubulointerstitial)

5

2 major causes of Acute Tubular Necrosis

ischemic & toxic

6

2-Pre-renal (inadequate blood supply) causes of dz

Heart failure - low cardiac out put - Low renal perfusion - Volume depletion - Sepsis - Severe bleeding

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3- Post-renal (bilateral urinary obstruction) causes of dz

Tumors, BPH ( prostate)

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: hematuria, proteinuria, hypertension

Acute nephritic syndrome:

8

AA (secondary) amyloid:

Amyloid precursor protein is an apolipoprotein produced by the liver as an acute phase reactant in response to long standing infection or inflammation

8

AA ( secondary amyloid ) seen in

Rheumatoid arthritis Behçet syndrome Crhon’s disease Osteomyelitis Tuberculosis Renal cell carcinoma Hodgkin’s disease

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A group of disorders associated with rapid decline in renal function with associated severe oliguria & if untreated death from renal failure within weeks to months

Rapidly progressive glomerulonephritis (RPGN)/ crescentic glomerulonephritis

9

Acute caues of Tubulointerstitial nephritis

Drugs(71%)

(antibiotics)

- Infection(15%)

- Idiopathic(8%)

- Sarcoidosis (1%)

10

Acute Drug Induced Interstitial Nephritis (AIN)

Pathogenesis:

Allergic type reaction ....manifested by

Interstitial infiltration of (eosinophils, lymphocytes, macrophages)

11

Acute Drug Induced Interstitial Nephritis

(AIN)Clinical presentations

Onset usually 2 weeks after start medication (first exposure) or

3-5 days if second exposure

Symptoms & Signs: ( allergic – type reaction) - Fever (27%)

- Rash (15%)

- Eosinophilia (23%)

- Triad of all (10%) or

- ARF / oliguria

- Asymptomatic

12

Acute injury to renal tubules, causing cell death (necrosis).....acute renal failure

Acute Tubular Necrosis (ATN)

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Acute pyelonephritis complications 

- Papillary necrosis

- Pyonephrosis

- Perinephric abscess

14

Acute pyelonephritis infections 

15

Acute pyelonephritis

pathogenesis:

Pathways of entry into kidney

1- Bloodstream: seeding of kidney from distant source

bacterial endocarditis, septicemia)

2- Ascending infection from lower urinary tract ( most common)

15

Acute pyelonephritis

Pathogenesis

Ascending infection:

Bacteria has to get into bladder first

Women:

Bacterial colonization of introitus & distal urethra....entry into bladder ( short urethra, foley's catheterization, sexual intercourse

Men:

entry into bladder ..BPH, catheterization, urine stasis...bacterial colonization...

Bacteria travel retrograde up the ureters to the kidneys ( vesicoureteral reflux)

15

Acute Pyelonephritis

laboratory findings

Elevated BUN, Creatinine (volume depletion) Elevated WBC

Pyuria, bacteruria,

WBC casts

16

Acute vs Late Post-Streptococcal glomerulonephritis pathogenesis

Initially : subendothelial IC deposits (activation of complement, influx of inflammatory cells with resultant proliferative GN…decline in GFR (fast clearance) Later: characteristic subepithelial “HUMPS”…responsible for epithelial cell damage & proteinuria (slow clearance)

17

Advanced sclerosing lupus nephritis Global sclerosis of >90% of glomeruli Advanced interstitial fibrosis & tubular atrophy Represents healing of prior inflammatory injury, advanced stages of chronic Class III, IV, V lupus nephritis

Class VI lupus nephritis

18

AIN serum levels 

** Blood Tests:

Increased BUN & creatinine

Increased eosinophils count

Tubular dysfunction: High K, low HCO3

19

AL (primary) amyloidosis

Amyloid precursor is light chain or fragment of light chain produced by abnormal clone of plasma cells Therefore, amyloid fibrils are composed of abnormal light chains Can occur alone or in association with multiple myeloma

19

AIN- laboratory assessment

Urine microscopy

Eosinophils

Sterile pyuria

WBC casts

Proteinuria (mild)

19

Alport Genetics

Mutations { COL4A4 & COL4A5 genes }

X-linked (80%) / AR & AD (20%)

20

Alport’s syndrome

Defects in

Collagen IV synthesis basement membrane