Vi. Renal Disease

Denielle Genesis B. Camato

VI. RENAL DISEASE ANALYSIS OF URINALYSIS AND BODY FLUIDS | REVIEWER

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GLOMERULAR

{ IMMUNOLOGIC DISORDERS: R Immune complexes (IgA) R Complement R Neutrophils R Lymphocytes R Cytokines

{ NON-IMMUNOLOGIC DISORDERS R Exposure to chemicals and toxins

{ SYSTEMIC DISORDERS R Nephrotic syndrome R Deposition of amyloid material from systemic

disorders that may involve chronic inflammation & acute-phase reactants

R The basement membrane thickening associated with diabetic nephropathy

v Viral respiratory infection v HIV v Hepatitis v Syphilis v LE v Strep Grp A infection

{ INSTERTITIAL { VASCULAR

q GLOMERULONEPHRITIS Sterile inflammatory process affects the glomerulus May find blood, protein, casts in urine

v Acute glomerular nepehritis (AGN) v Chronic glomerular nephritis (CGN) v Renal failure

q ACUTE STREPTOCOCCAL GLOMERULONEPHRITIS Symptoms usually occur in children and young adults

ffg respiratory infection Elevated BUN Usually with Group A strep infection ; EDEMA most

noticeably around the eyes ASO titer ; provides evidence that the disease is of

streptococcal origin

q RAPIDLY PROGRESSIVE (CRESCENTIC) GLOMERULONEPHRITIS RPGN Most serious form of acute glomerular disease Poor prognosis [renal failure Deposition of immune complexes in the glomerulus;

accompanied by other immune systemic disorder (SLE) Elevated protein levels and low glomerular filtration

rate Increased fibrin degradation products, cryoglobulins,

deposition of IgA immune complexes

q GOOD PASTURES SYNDROME Appearance of cytotoxic autoantibody against the

glomerular and alveolar basement membranes (antiglomerular basement membrane antibody); can be detected in patient serum

Morphologic changes to the glomeruli resembling the RGPN

Initial pulmonary complaints: HEMOPTYSIS and DYSPNEA [ development of hematuria

VASCULITIS

WEGENERs Granulomatosis HENOCH-SCHONLEIN purpura (latin word, purple) red or purple

discolorations: Bleeding under the skin

q WEGENERS GRANULOMATOSIS Granuloma-producing inflammation of the small blood

vessels Diagnosis: ANTINEUTROPHILIC CYTOPLASMIC

ANTIBODY (ANCA) in patients serum Binding these autoantibodies to the neutrophils located

in the vascular walls may initiate the immune response & the resulting granuloma formation; elevated BUN & CREATININE

q HENOCH-SCHONLEIN PURPURA Occurring primarily in children following upper

respiratory infections Raised, red patches on skin Respiratory and gastrointestinal symptoms; Blood in

sputum and in stools Proteinuria & hematuria with RBC casts; complete

recovery is seen in more than 50% patients

q IMMUNOGLOBULIN A NEPHROPATHY Also known as the Bergers disease, IgA nephropathy;

IgA complexes are deposited on the glomerular membrane most common cause of glomerulonephritis

Patients have increased serum levels of IgA; may result to mucosal infection

Seen in young children & young adults Macroscopic hematuria; patient may remain

asymptomatic for 20 years or more Gradual progression to chronic glomerulonephritis and

ESRD

q MEMBRANOUS GLOMERULONEPHRITIS Thickening of the glomerular basement membrane

resulting from the deposition of immunoglobulin G immune complexes.

Frequent development of nephrotic syndrome; tendency towards thrombosis

E Sjorens syndrome Secondary syphilis, Hepa B, Gold & Mercury

treatments; Microscopic hematuria, elevated urine protein

q MEMBRANOPROLIFATIVE GLOMERULONEPHRITIS (MPGN) TYPE 1 Displays increased cellularity in the

subendothelial cells of the mesangium (interstitial area of the Bowmans capsule) causing thickening of the capillary walls [ nephrotic syndrome

TYPE 2 Displays extremely dense deposits in the

glomerular basement membrane [ chronic glomerulonephritis



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q CHRONIC GLOMERULONEPHRITIS Gradually worsening symptoms [ fatigue, anema,

hypertension, edema, oliguria Hematuria, gulcosuria (tubular dysfunction), varieties of

cast including BROAD CASTS. Increased BUN, CREATININE, electrolyte imbalance

q NEPHROTIC SYNDROME Marked by massive proteinuria (greater than 3.5g/dL),

low levels of serum albumin, high levels of serum lipids, and pronounce edema.

Acute onset of the disorder [ systemic shock; decreases blood pressure (hypotension) and flow of blood in the kidney

Ensuing hypoalbuminemia appears to stimulate the increased production of lipids by the liver

Lower oncotic pressure in the capillaries resulting from the depletion of plasma albumin increases of the loss of fluid in the interstitial spaces which is accompanied by sodium retention thus producing edema

Urinalysis: proteinuria, fat droplets, oval fat bodies, RTE cells, fatty & waxy cats, microscopic hematuria.

q MINIMAL CHANGE DISEASE Also known as LIPID NEPHROSIS PODOCYTES appear to be less tightly fitting allowing for

the increased filtration of protein Allergic reactions, recent immunization & possession of

the HUMAN LEUKOCYTE ANTIGEN B-12 (HLA -12) have been associated

Prognosis is good, disease respond to corticosteroids

q FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS) Affects only certain areas of glomeruli & others

remain normal Often seen in association with abuse of heroin &

analgesics

q TUBULAR DISORDERS Actual damage to the tubules; hereditary disorder that

affects intricate functions of the tubules

q ACUTE TUBULAR NECROSIS (ATN) Primary disorder to the tubule; causes ischemia; lack of

oxygen presentation to the tubules SHOCK= Cardiac failure, sepsis involving toxigenic

bacteria, anaphylaxis, massive hemorrhage, contact with high voltage electricity

Proteinuria, microscopic hematuria, RTE cells, granular cast, waxy, broad cast

q HEREDITARY & METABOLIC TUBULAR DISORDER FANCONIS SYNDROME- frequently associated with

tubular dysfunction; failure of tubular reabsorption in the proximal convoluted tubule.

PCT glucose, amino acids, phosphorus, sodium, potassium, HCO3, H20

May be inherited in association in cystinosis & HARTNUP DISEASE

Exposure to toxic agents; complication of multiple myeloma & renal transplant

q INTERSITIAL DISORDER TUBULOINTERSTITIAL DISEASE; close proximity

between renal tubules & renal instertitium. UTI most common renal disease; may involve the lower

urinary tract (URETHRA & BLADDER) or the upper urinary tract (RENAL PELVIC, TUBULES, & INSTERTITIUM); reveals presence of numerous WBCs & bacteria often accompanied by mild proteinuria & hematuria & an increased in pH

CYSTITIS- infection of the bladder is most common encountered.

q ACUTE PYELONEPHRITIS Infection of the upper urinary tract including both the

tubules & instertitium is termed as pyelonephritis and can occur both in acute & chronic form

Bacteria ascending from a lower UTI into the renal tubules and instertitum

Obstructions renal calculi (stones) visicouretral reflux- reflux of the urine from the

bladder back into the ureters Appropriate antibiotic therapy

q CHRONIC PYELONEPHRITIS Recurrent infection; more serious disorder can result in

permanent damage to the tubules & possible progression to chronic renal failure

CONGENITAL URINARY STRUCTURAL defects producing REFLUX NEPHROPATHY are the most frequent cause

Often diagnosed in children

q ACUTE INSTERTITIAL NEPHRITIS (AIN) Inflammation of the renal instertitium followed by

inflammation of the tubules. Fever & skin rash are frequent initial symptoms AIN is primarily associated with an allergic reaction to

medications that occurs within the renal instertitium; possible binding of the medication to instertitial protein

Penicillin, methicillin, ampicillin, cephalosporin, sulphonamides, thiazide diuretics

URINALYSIS: hematuria, proteinuria, numerous WBCs, WBC casts

LEUKOCYTE STAINING for the presence of increased Eosinophils maybe useful to confirm diagnosis

Treatment: corticosteroids

q VASCULAR DISORDERS Disorders include autoimmune disorders, vasculitis, and

diabetes mellitus that affects integrity of the renal blood vessels.



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q RENAL FAILURE Maybe in acute or chronic form; gradual progression

to chronic renal failure or ESR ESRD decrease in glomerular filtration rate;

steadily rising of BUN & CREA (azotemia), electrolyte imbalance, lack of concentrating ability producing an isosthenuric urine, proteinuria, glycosuria, granular, waxy, broad cast

ACUTE RENAL FAILURE (ARF) exhibits sudden loss of renal function & is frequently

reversible

PRE-RENAL sudden decrease in renal blood flow to the kidney

(haemorrhage, burns, surgery, septicemia)

RENAL acute glomerular and tubular disease, acute

pyelonephritis, acute instertitial nephritis

POST RENAL renal calculi, tumors, obstructions, crystallization of

ingested substance

RENAL LITHIASIS stones may form in the CALYCES and PELVIS of the

kidney, ureter, and bladder. Small stone may pass by in urine thereby causing severe pain but larger stones cannot

Lithotripsy

procedure using high energy shock waves that can be used to break stones located in the upper urinary tract into pieces that can be passed in the urine; SURGICAL removal can also be employed

approximately 75% of stones are composed of CAOX or PHOSPHATE.

Magnesium ammonium phosphate (STUVITE), uric acid, and cysteine are the other primary calcul i constituents.

Vi. Renal Disease

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