GLOMERULAR DISORDERS

DISORDERS ETIOLOGY CLINICAL COURSE FINDINGS

Acute Poststreptococcal Deposition of immune complexes formed Rapid onset of hematuria and Macroscopic hematuria
Glomerulonephritis in conjunction with group A edema; permanent renal damage Dysmorphic RBCs
(APGN) Streptococcus infection, on the seldom occurs. RBCs Casts
glomerular membranes. Granular Casts
(+) ASO Titer
↑ BUN
Rapidly Progressive Deposition of immune complexes from Rapid onset with glomerular Macroscopic hematuria
Glomerulonephritis systemic immune disorders on the damage and possible progression Proteinuria
(Crescentic Glomerulonephritis) glomerular membrane. to end stage renal failure. RBC Casts
SLE (Systemic Lupus Erythematosus) ↑ fibrin degradation products,
Production of Crescentic cryoglobulins, IgA immune
Formations containing complexes in glomerulus
macrophage, fibroblasts,
polymerized fibrins
Goodposture Syndrome Attachment of a cytotoxic antibody Hemoptysis and dyspnea Macroscopic hematuria
formed during viral respiratory infections followed by hematuria; Possible Proteinuria
to glomerular and alveolar basement progression to end stage renal RBC Casts
membranes. failure.

Deposition of antiglomerulus basement

membrane antibody to glomerular and
alveolar basement membranes.

Wegener's Granulomatosis Antineutrophilic Cytoplasmic Pulmonary symptoms including Macroscopic hematuria

Autoantibody (ANCA) binds to hemoptysis developed first Proteinuria
neutrophils in vascular walls producing followed by renal involvement RBC Casts
damage to small vessels in the lungs and and possible progression to end -
 glomerulus.
Henoch-Schonlein Purpura Occurs primarily in children following
viral respiratory infections
Decrease in platelets disrupts vascular
integrity.
Membranous Thickening of the glomerular membrane
Glomerulonephritis following IgG immune complex
deposition associated with systemic
disorders
Membranoproliferative Cellular proliferation affecting the
Glomerulonephritis capillary walls or the glomerular
(MPGN) membrane basement membrane,
possibly immune mediated.
Associated with autoimmune disease,
infection and malignancies
Chronic Glomerulonephritis Marked decrease in renal function
resulting from glomerular damage
precipitated from by other renal
disorders.
IgA Nephropathy Deposition of IgA on the glomerular
(Berger’s Disease) membrane resulting from increased
levels of serum IgA.
Nephrotic Syndrome Disruption of electrical charges that
stage renal failure.
Initial appearance of purpura Macroscopic hematuria
followed by blood in sputum and Proteinuria
stools and eventual renal RBC Casts
involvement.
Complete recovery is common,
but may progress to renal failure.
Slow progression to nephrotic Macroscopic hematuria
syndrome or possible remission; Proteinuria
tendency of Thrombosis.
Slow progression to chronic Hematuria
glomerulonephritis (Type 2) or Proteinuria
nephrotic syndrome (Type I). Tram-Track appearance
Noticeable decrease in renal Hematuria
function progressing renal failure. Proteinuria
Glucosuria
Cellular and Granular Casts
Waxy and Broad Casts
Recurrent macroscopic hematuria Early stage: Hematuria
following exercise with slow Late Stage: See Chronic
progression to chronic Glomerulonephritis
glomerulonephritis.
Acute onset following systemic Heavy Proteinuria
 produce the tightly fitting podocyte shock Microscopic Proteinuria Renal
barrier resulting in massive loss of Tubular Cells (RTE)
proteins and lipids. Oval fat bodies
Fat droplets
Fatty and Waxy Casts

Blood: Decrease Albumin

Urine: Increase Albumin
Minimal Change Disease Disruption podocytes occurring primarily Frequent complete remission Heavy Proteinuria
(Lipoid Nephrosis, Nil Disease) in children following allergic reactions following corticosteroid Transient hematuria
and immunizations. treatment. Fat droplets

Focal Segmental Disruption of podocytes in certain areas May resemble nephrotic Proteinuria
Glomerulosclerosis of glomeruli associated with heroin and syndrome or minimal change Hematuria
(FSGS) analgesic abuse and AIDS. disease.

Alport Syndrome Genetic disorder showing lamellated and Slow progression to nephrotic Same with Nephrotic
thinning of glomerular basement syndrome and end stage renal Syndrome
membrane. disease.

Diabetic Nephropathy Believed to be associated with Develops Sclerosis Indicator: Microalbuminuria

(Kimmelsteil - Wilson Disease) deposition of glycosylated proteins Modification of diet and strict (+) Red color in Micral Test
resulting from poorly controlled blood control of hypertension
glucose level.

Most common cause of end stage RENAL

DISEASE
 TUBULAR DISORDERS
DISORDERS ETIOLOGY
Acute Tubular Necrosis Damage to the renal tubular
cells caused by ischemia or
toxic agents.
Fanconi Syndrome Inherited in association with
cystinosis and Hartnup disease tubular reabsorption requiring
or acquired through exposure
to toxic agents.
Uromodulin-associated kidney Inherited defect in the
disease (UKD) production of normal
uromodulin by the renal
tubules and increased uric acid
causing gout
Nephrogenic Diabetes Inherited defect of tubular Requires supportive therapy to
Insipidus response to ADH or acquired
from medications.
Renal Glucosuria Inherited autosomal recessive
trait
Defective tubular reabsorption
of glucose
CLINICAL COURSE FINDINGS
Acute onset of renal Microscopic hematuria
dysfunction usually resolved Proteinuria
when the underlying cause is RTE Cells, RTE Casts
corrected. Hyaline, granular, waxy, broad
casts
Generalized defect in renal Glucosuria
Possible cystine crystals
supportive therapy.
Continual monitoring of renal RTE Cells
function for progression of Hyperuricemia
renal failure and possible
kidney transplantation
Low SG
prevent dehydration. Polyuria
Pale yellow colored urine
False-negative results of
chemical tests
Benign disorder Glucosuria
Increase urine glucose
Normal blood glucose
 INTERSTITIAL DISORDERS
DISORDERS ETIOLOGY CLINICAL COURSE FINDINGS
Cystitis Ascending bacterial infection Acute onset of urinary WBCs, Bacteria
(LOWER UTI) of the bladder. frequency and burning Microscopic Hematuria
resolved with antibiotics Mild Proteinuria
Most frequently encountered. Increased pH
NO CASTS
Most common WOMEN and
CHILDREN.

UTI- most common renal

disease
*LOWER UTI: urethra &
Bladder
*UPPER UTI: Renal pelvis,
tubules, interstitium

Acute Pyelonephritis Infection of the renal tubules Acute onset of urinary WBCs, Bacteria
(UPPER UTI) and interstitium related to frequency, burning and lower WBC Casts
interference of urine flow to back pain resolved with Bacterial Casts
the bladder, reflux of urine antibiotics. Microscopic Hematuria
from the bladder, and Proteinuria
untreated cystitis.

Chronic Pyelonephritis Recurrent infection of the Frequently diagnosed in WBCs, Bacteria

tubules and interstitium children; Requires correction WBC Casts
caused by structural of the underlying structural Bacterial Casts
abnormalities affecting the defect and possible Granular Casts

Acute Interstitial Nephritis
flow of urine.
Allergic inflammation of the
renal interstitium in response
to certain medications.
progression to renal failure. Waxy and Broad Casts
Hematuria
Proteinuria
Acute onset of renal WBCs (Increase Eosinophils)
dysfunction often WBC Casts
accompanied by a skin rash; NO Bacterial Casts
Resolves following Hematuria
discontinuation of medication Proteinuria
and treatment with
corticosteroids