Renal involvement usually follows a protracted course with periods of remissions and exacerbations (On & Off) immunosuppressive therapy
Lupus nephritis
* In situ Immune Complex (Ag-Ab) formation
Fixed antigens ( intrinsic)/ anti GBM nephritis) Planted antigens (exogenous/ endogenous)
*Conditions associated with IgA nephropathy
Hepatic cirrhosis - Gluten enteropathy - HIV infection - Minimal change disease -Others: membranous, Wegener’s, Ankylosing spondylitis, small cell Ca
*75% of all bladder tumor
Urothelial carcinoma
Papillary carcinoma
-Dysuria, frequency, urgency -Low back/ pelvic or genital pain -Fever, Chills & leukocytosis -Loss of sex drive,
- painful erections / ejaculation *DRE: enlarged tender prostate
Prostatitis
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
1-Renal ( primary kidney diseases)
Congenital - Acquired (glomerular / tubulointerstitial)
2 major causes of Acute Tubular Necrosis
ischemic & toxic
2-Pre-renal (inadequate blood supply) causes of dz
Heart failure - low cardiac out put - Low renal perfusion - Volume depletion - Sepsis - Severe bleeding
3- Post-renal (bilateral urinary obstruction) causes of dz
Tumors, BPH ( prostate)
: hematuria, proteinuria, hypertension
Acute nephritic syndrome:
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
AA ( secondary amyloid ) seen in
Rheumatoid arthritis Behçet syndrome Crhon’s disease Osteomyelitis Tuberculosis Renal cell carcinoma Hodgkin’s disease
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
Acute caues of Tubulointerstitial nephritis
Drugs(71%)
(antibiotics)
- Infection(15%)
- Idiopathic(8%)
- Sarcoidosis (1%)
Acute Drug Induced Interstitial Nephritis (AIN)
Pathogenesis:
Allergic type reaction ....manifested by
Interstitial infiltration of (eosinophils, lymphocytes, macrophages)
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
Acute injury to renal tubules, causing cell death (necrosis).....acute renal failure
Acute Tubular Necrosis (ATN)
Acute pyelonephritis complications
- Papillary necrosis
- Pyonephrosis
- Perinephric abscess
Acute pyelonephritis infections
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)
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)
Acute Pyelonephritis
laboratory findings
Elevated BUN, Creatinine (volume depletion) Elevated WBC
Pyuria, bacteruria,
WBC casts
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)
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
AIN serum levels
** Blood Tests:
Increased BUN & creatinine
Increased eosinophils count
Tubular dysfunction: High K, low HCO3
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
AIN- laboratory assessment
Urine microscopy
Eosinophils
Sterile pyuria
WBC casts
Proteinuria (mild)
Alport Genetics
Mutations { COL4A4 & COL4A5 genes }
X-linked (80%) / AR & AD (20%)
Alport’s syndrome
Defects in
Collagen IV synthesis basement membrane
