SEM 4
RENAL DISEASES
Kidney – filtration (removal of waste
products – consistently exposed to
damaging substances)
A. Glomerular Disorders
Can be categorized as:
1. Immunologic = deposition of
immune complexes – ex.
Complement, WBCs, cytokines –
when attached to glomerular
membrane there will be changes or
damage the membrane
2. non-immunologic = damaged
membrane due to deposition of
chemicals and toxins
- Glomerulonephritis
- Acute Post-streptococcal
Glomerulonephritis
- Rapidly Progressive (Crescentic)
Glomerulonephritis
- Goodpasteur’s Syndrome
- Vasculitis
- Immunoglobulin A Nephropathy
- Membranous Glomerulonephritis
- Membranoproliferative
Glomerulonephritis
- Chronic glomerulonephritis
- Nephrotic syndrome
- Minimal Change Disease
- Focal Segmental Glomerulosclerosis
B. Tubular disorders
- Acute tubular necrosis
- Hereditary and Metabolic Tubular
Disorders
C. Interstitial disorders
- Acute pyelonephritis
- Chronic pyelonephritis
- Acute interstitial nephritis
D. Vascular disorders
E. Renal failure
F. Renal lithiasis
GLOMERULAR DISORDERS
•Immune origin
• Effects
*Majority is from immune complexes
A. cellular infiltration or proliferation
B. thickening of the glomerular basement
membrane
*Glomerulonephritis:
- sterile, inflammatory process that affects
the glomerulus and is associated with the
finding of blood, protein, and casts in the
urine (hematuria, proteinuria)
- rapidly progressive (acute-chronic-
necrotic-renal failure)
A. ACUTE GLOMERULONEPHRITIS
• Symptoms: edema (most evident in the
eyes), fatigue, hypertension, oliguria, and
hematuria
• Group A streptococcus that contain M
protein in the cell wall
• Elevated ASO (Anti Streptolysin O) titer
provides evidence it is of streptococcal origin
*AGN post infection = sequalae=
Streptococcus pyogenes = virulence factor
(M protein) = some complexes attached to
glomerular membrane = major caus of strep
throat
ASO (Anti Streptolysin O) - also a virulence
factor which is an immunologic – from
bacteria
*Children and young adults
* When toxicity subsides, the macroscopic
results in urine will return to normal (Early
phase of convalescence). But microscopic
hematuria will still be present until the
glomerular is repaired. (INCREASE BUN)
 B. RAPIDLY PROGRESSIVE • Symptoms: hemoptysis
(CRESCENTIC) (blood in sputum) and dyspnea (difficulty in
GLOMERULONEPHRITIS breathing) = respiratory infection followed
by hematuria
*RSV, Corona, Adeno
Viral infection = strengthens your immune
system = antibodies = can be cytotoxic to
damage the glomerulus – AUTOIMMUNE
DISORDER
• Systemic lupus erythematosus as the most
common immune disorder. D. WEGENER’S GRANULOMATOSIS
• Symptoms are initiated by deposition of
immune complexes in the glomerulus.
Damage by macrophages to the capillary
walls releases cells and plasma into the
Bowman’s space, and the production of
crescentic formations containing
macrophages, fibroblasts, and polymerized
fibrin • A granuloma-producing
*NOT FROM INFECTION inflammation of the small blood
*poorer prognosis = the crescentic vessels of primarily the kidney and
formation will lead to permanent damage to respiratory system.
the capillary tuft of the glomerulus *Granuloma = autoantibodies +
*PLASMA = INCREASE PROTEIN = DECREASE neutrophil + vascular wall or lungs
GFR = INCREASE FDPs = DETECT IGA • Key to diagnosis: demonstration of
IMMUNE COMPLEXES AND the ANCA in the patient serum –
CRYOGLOBULINS indirect immunofixation (px serum +
*TO CONFIRM WHETHER IT IS ACUTE OR ethanol/formalin) – positive result
CHRONIC = BIOPSY having perinuclear pattern (PANTA)
– fixed with ethanol (PANTA)
C. GOODPASTURE’S SYNDROME - Fixed with formalin (CANTA) –
GRANULAR THROUGHOUT THE
CYTOPLASM
• Symptoms: patients usually present
pulmonary symptoms and later
develop to renal involvement.
*ELEVATED BUN AND CREATININE

• Anti-glomerular basement membrane E. HENOCH-SCHONLEIN PURPURA

antibody: autoantibodies - serum
Attachment of an autoantibody to the
basement membrane followed by
complement activation that produces
capillary destruction.
 Symptoms: the appearance of raised G. MEMBRANOUS
red patches on the skin; the GLOMERULONEPHRITIS
presence of hemoptysis and
dysenteric stools (blood in stool).
• Renal involvement is the most
serious complication of the disorder
and may range from mild to heavy
proteinuria and hematuria with RBC
cast. •Associated with systemic lupus
*Usually after the upper respiratory erythematosus, Sjogren’s syndrome,
infection secondary syphilis, hepatitis B, gold and
DIFFERENCE BETWEEN GOOD mercury treatment, and malignancy.
PASTEUR: DECREASE PLATELETS – • Type I: shows increased cellularity in
PURPURA the subendothelial cells of the
Respiratory and gastrointestinal mesangium, causing thickening of the
symptoms capillary walls.
*Patient progress to nephrotic
F. IgA NEPHROPATHY syndrome
• Type II: displays extreme dense
deposits in the basement glomerular
membrane.
*Patient progress to chronic
glomerulonephritis

H. CHRONIC GLOMERULONEPHRITIS
• AKA Berger’s disease, a disorder common
among children and young adults.
• A patient with this disorder may remain
essentially asymptomatic for 20 years or
more, however, there is gradual
progression to chronic glomerulonephritis
and end-stage renal disease.
*INCREASE IGA IN THE BLOOD • Shows worsening symptoms include
URINE – ULTRAFILTRATE OF PLASMA fatigue, anemia, hypertension, edema,
EXCESS – FILTRATED BY KIDNEYS and oliguria.
IGA IS LARGE IMMUNOGLOBULIN – • Patient shows marked decrease in GFR
DEPOSITED IN THE FILTER (GLOMERULUS) with increased BUN and creatinine.
*Strenous exercise, mucosal infections *1-7 can all progress to chronic
*worsening symptoms/poor prognosis
I. NEPHROTIC SYNDROME
• Increased permeability of the
glomerular membrane is attributed
to damage to the membrane and
changes in the electrical charges in
the basal lamina and podocytes,
producing a less tightly connected
barrier common during systemic
shock.
• Albumin is primarily depleted.
• Depletion of immunoglobulins and
coagulation factors -> risk of
infection and coagulation disorders.
*Podocytes barrier is destroyed
J. MINIMAL CHANGE DISEASE
• AKA Lipid nephrosis, produces little
cellular damage to the glomerulus.
• Etiology is unknown but it is
associated with allergic reactions,
recent immunization, and
possession of the human leukocyte
antigen-B12 (HLA-B12).
*NON-SPECIFIC
K. FOCAL SEGMENTAL
GLOMERULOSCLEROSIS
• Affects only certain numbers and
areas of glomeruli (undamaged),
and the others remain normal.
• Immune deposits, primarily
immunoglobulins M and C3, are a
frequent finding and can be seen in
undamaged glomeruli.
• Often seen in association with
abuse of heroin and analgesics and
persons with AIDS.
*CHEMICALS/TOXINS
*Other functions are normal
*Similar symptoms to minimal
change disease and nephrotic
syndrome = same problem with
podocyte
TUBULAR DISORDERS
A. ACUTE TUBULAR NECROSIS
• Disorders causing ischemic ATN
include shock, trauma, such as
crushing injuries, and surgical
procedures.
• Nephrogenic agents can
damage and affect function of
the RTE cells. (CONVOLUTED OR
DISTAL) (e.g. aminoglycosides,
antifungal agents,
amphotericin, cyclosporine,
radiographic dye, organic
 solvents like ethylene glycol,
heavy metals, and mushroom
poisoning = Nephrogenic agents
B. FANCONI’S SYNDROME
• There is generalized failure of tubular
reabsorption in the PCT.
• Substances most noticeably affected
include glucose, amino acids, phosphorus,
sodium, potassium, bicarbonate, and water.
• Heavy metals and outdated tetracycline,
or as complication of multiple myeloma
(altered plasma proteins) and
renal transplant.
*PCT – important in concentration of urine
C. CYSTITIS
• If left untreated can progress to more
serious upper UTI.
• More common among females and
children.
*BACTERIAL INFECTION
D. ACUTE PYELONEPHRITIS
• Most frequently occurs as a result of
ascending movement of bacteria from a
lower UTI into the renal tubules and
interstitium.
• Conditions that interfere downward flow
of urine from the ureter to the bladder or the
complete emptying of the bladder during
urination include presence of renal calculi,
pregnancy, and visicoureteral reflux.
*Reflux of urine = untreated cystitis
E. CHRONIC PYELONEPHRITIS
• Often results to permanent
damage to the renal tubules and
possible progression to chronic
renal failure.
• Congenital urinary structural
defects producing a reflux
nephropathy are the most
common cause.
F. ACUTE INTERSTITIAL NEPHRITIS
• Often marked by inflammation
of the renal interstitium
followed by inflammation of the
renal tubules.
• Medications associated with
AIN include penicillin,
methicillin,
ampicillin, cephalosporins,
sulfonamides, NSAIDs, and
thiazide diuretics.
• Discontinuation of the
offending medication frequently
 results to normal renal function.
However, supportive renal
dialysis may be required to some
patients.

VASCULAR DISORDERS
*Tissues surrounding our kidneys
- Autoimmune disease
- Vasculitis
- Diabetes Mellitus
*Renal ischemia and loss of functional renal
tissue
RENAL FAILURE
Progression to end-stage renal disease is
characterized by
*It can start from acute or chronic forms;
progressive or gradual
• Marked decrease in glomerular filtration
rate (< 25ml/min)
• Azotemia; BUN and CREATININE are
STEADILY RISING
• Electrolyte imbalance
• Lack renal concentrating ability
• Proteinuria
• Renal glycosuria
• Presence of telescoped urine sediment
(granular, waxy, and broad cast)
*ACUTE RENAL FAILURE (ARF) – SUDDEN
LOSS OF RENAL FUNCTION BUT REVERSIBLE
- PRE-RENAL: sudden decrease of blood flow
to the kidneys, RENAL: acute
glomerular/tubular diseases (AGN, CGN,
ATD), POST RENAL = tumor/tumor
obstructions, presence of renal calculi
* CHRONIC RENAL FAILURE (CRF) –
GRADUAL LOSS OF RENAL FUNCTION BUT
IRREVERSIBLE – rely on DIALYSIS
RENAL LITHIASIS
Renal calculi may form in the calyces and
pelvis of the kidney, uterus, and bladder
*STONES IN VARIOUS SIZES ON KIDNEYS
*SMALL CALCULI- pass through on the urine;
px experience pain – lower back pain
*LARGE CALCULI – cannot pass through;
cannot be detected until form a urinary
obstruction (no S/S at first)
Lithotripsy: a procedure that uses high-
energy shock waves, than can be used to
break stones located in the upper urinary
tract so that they can be passed in the urine
Analysis of Chemical Composition of renal
calculi
75%: calcium oxalate or phosphate –
metabolic and phosphate disorders/diet
: Magnesium ammonium phosphate
(struvite) – UTI (involving urea splitting
bacteria) , uric acid (diet,inc high purine
content= samgyupsal, beans, ACIDIC PH)
and cystine (METABOLISM DISORDER)
pH= alkaline higher than 7.0