Renal Review Flashcards
Define Azotemia
2 lab changes
Represents what change
3 Forms
Lab Test Abnormality
Elevated Creatinine and BUN
Represents Decrease in GFR
Pre-Renal, Renal, Post-Renal
Define Uremia
Signs and symptoms secondary to azotemia
3 signs of uremia
Gastroenteritis
Neuropathy
Fibrinous pericarditis
Anti-GBM antibodies give us what two diseases
Anti-GBM disease
Goodpasture’s
Anti-Megalin like antibodies gives what disease
Appearance
Membranous GN
Granular pattern
Cell-mediated injury appears how?
Associated with what
Pausi-Immune appearance
RPGN
Renal Ablation Glomerulopathy define
Start losing nephrons and reach 50% you damage the remaining and progress to renal failure
Define Nephrotic Syndrome
Loss of glomeruli –> Can’t filter –> Lose protein
3 Blood/urine findings of Nephrotic
1 physical finding
Proteinuria > 3.5/day
Hypoalbuminemia <3 gram
Lipidemia
Edema due to low albumin
Number systemic disease cause of nephrotic syndrome?
Diabetes mellitus
A child presents with proteinuria of mainly albumin. There are no changes under LM. Under EM, we see an effacement of foot processes. IF finds nothing. Steroids prescribed have had a benefit.
Minimal Change Disease
Caucasian adult presents with proteinuria. LM shows thickened capillary walls. EM shows thickened BM, subepithelial deposits, and effacement of foot processes. IF shows granular subepithelial deposits. Silver stain LM deposits show a spike-and-dome appearance. Anti-Megalin-like antibodies are found
Membranous Nephropathy
African-American presents with non-selective proteinuria and hypertension. Some glomeruli deisplay partial sclerosis under LM. Injury of visceral epithelial cells is documented. Patient is a HIV individual with a history of IV heroin use. Disease does not respond well to steroids.
FSGS
Patient presents with microscope ifndings of thickened BM, proliferating mesangial cells and matrix. LM shows a tram-track appearance of BM with PAS and silver stains. Patient has hepatitis B. EM shows subendothelial deposits of C3 and IgG.
Type 1 Membranoproliferative Glomerulonephritis
Patient presents with microscope ifndings of thickened BM, proliferating mesangial cells and matrix. LM shows a tram-track appearance of BM with PAS and silver stains. Patient has hepatitis C. EM shows lamina densa deposits of electron-dense material.
Type 2 Membranoproliferative Glomerulonephritis
4 Findings of Nephritic Syndromes
- Hematuria
- Oliguria
- Azotemia
- HTN
3 Morphological signs of Nephritic syndromes
- Proliferation of glomerular cells
- Inflammatory cells in glomerulus
- RBC casts in urine
Child presents with dark colored urine and is hypertensive with some periorbital edema. He had a sore throat that cleared up 2 weeks ago. Anti-streptolysin O and anti-DNAase tests are positive.
Post Streptococcal GN
Patient presents with a rapid loss of renal function. Crescents are found in Bowman’s space on microscopy. Anti-GBM antibodies with linear IgG deposition. Pulmonary hemorrhaging has been occurring.
Type 1 RPGN with Goodpasture’s
Patient presents with a rapid loss of renal function. Crescents are found in Bowman’s space on microscopy. IF shows immune complex deposition in granular pattern.
Type 2 RPGN
Patient presents with a rapid loss of renal function. Crescents are found in Bowman’s space on microscopy.Vasculitis is seen. IF is negative. ANCA positive
Type 3 RPGN
Young healthy patient presents with hematuria and reports a recent GI/UR infection. Patient has also been diagnosed recently with Henoch-Schonlein Purpura. Staining shows IgA deposits in mesangium.
IgA Disease/Berger’s Disease
Young adult male patient presents with hematuria, deafness, and eye disturbances. It is determined he has a X-linked mutation for alpha5 chain of type IV collagen.
Alport Syndrome/Hereditary Nephritis
Patient presents with hematuria but recovers quickly. Patient has heterozygous genotype for abnormality in type IV collagen.
Benign Familial Hematuria/ Thin Basement Membrane Disease
Patient presents with microtubular arrays, deposits throughout the kidney, wire loops, and Full House IF staining. Immune complex deposition is determined to be the underlying pathology.
SLE Nephropathy
This is the #1 cause of end stage renal disease in US
Diabetic Associated Renal Disease
This is the #1 cause overall for nephrotic syndrome in adults in US.
Diabetic Associated Renal Disease
Patient presents with Nodular glomerulosclerosis with Kimmelstiel-Wilson nodules on staining.
Glomerular Disease of Diabetic Associated Renal Disease
Patient presents with hyaline arteriolosclerosis.
Renal Arteriolosclerosis of Diabetic Associated Renal Disease
Patient presents with increased infections from glycosuria, bladder stasis, and altered immune status.
Pyelonephritis of Diabetic Associated Renal Disease
This is the most common cause of papillary necrosis
Diabetes
Patient presents with deposits in glomeruli that has damaged all glomeruli equally. The damage began in the mesangium. The deposits stain salmon pink under Congo Red Stain and apple green birefringence on polarization.
Amyloidosis
Patient with existing multiple myeloma presents with nodular pattern of deposition under LM. Bence Jones proteins are detected in urine. IF shows high Kappa Light chain deposition.
Light Chain Deposition Disease
Patient with existing multiple myeloma presents with renal dysfunction due to giant cell reaction around distal tubules. Distal tubules are shown to have light chain casts with TH protein involved.
Light Chain Cast Nephropathy
Patient with Hepatitis C presents with palpable purpura, arthralgias and Raynaud’s. Histology shows circulating immunoglobulins that precipitate when cool and become soluble when warm.
Cryoglobulinemic Nephritis
Patient presents with nephrotic syndrome that looks like amyloid but does not stain amyloid.
Fibrillary Immunotactoid glomerulonephritis
African-American presents with FSGS of the collapsing variant.
HIV nephropathy
Patient rejects a kidney transplant on the operating table.
Hyperacute Rejection
Patient rejects a kidney transplant due to preformed antibodies against the graft.
Hyperacute Rejection
Patient has CD8 cytotoxic T cells attack the endothelial cells of his or her kidney transplant.
Acute - Cellular
Patient has rejection vasculitis months after transplant of new kidney.
Acute - Humoral
Patient presents with a slow steady increase in serum creatinine while slowly losing renal function.
Chronic
Patient presents years after kidney transplant and is now seeing a loss in tissue of his transplant. He was immunosuppressed heavily during his transplant surgery.
Polyoma Virus (BK)
Patient presents with a rapid decline in renal function over 24 hours. Urine Cr is greater than 100. FE Na+ is less than 1%. Urine Na is less than 20. BUN/Creatinine is greater than 20:1. Specific gravity is higher than normal.
What is treatment
Pre-Renal ARF
Hydration/Volume expansion
Patient presents with a rapid decline in renal function over 24 hours. Urine Cr is less than 70. FE Na+ is greater than 3%. Urine Na is greater than 30.
What is treatment
Renal ARF
Supportive (NOT HYDRATION)
Patient presents with rapid decline in renal function over 24 hours. A surgical operation cures the problem.
Post-Renal ARF.
Patient presents with hypertension and uremia. GFR is less than 20% of normal. Ultrasound shows small kidneys. Blood tests show anemia, metabolic acidosis, and secondary hyperparathyroidism. Bleeding disorder is present as well.
Chronic Renal Failure
Hospitalized patient presents with a reduction of renal function. Morphologically there is evidence of tubular injury with tubular cell casts in urine. Patient tests positive for hypotension and toxins.
Acute Tubular Necrosis
