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Flashcards in Renal Review Deck (48)
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1
Q

Define Azotemia
2 lab changes
Represents what change
3 Forms

A

Lab Test Abnormality
Elevated Creatinine and BUN
Represents Decrease in GFR
Pre-Renal, Renal, Post-Renal

2
Q

Define Uremia

A

Signs and symptoms secondary to azotemia

3
Q

3 signs of uremia

A

Gastroenteritis
Neuropathy
Fibrinous pericarditis

4
Q

Anti-GBM antibodies give us what two diseases

A

Anti-GBM disease

Goodpasture’s

5
Q

Anti-Megalin like antibodies gives what disease

Appearance

A

Membranous GN

Granular pattern

6
Q

Cell-mediated injury appears how?

Associated with what

A

Pausi-Immune appearance

RPGN

7
Q

Renal Ablation Glomerulopathy define

A

Start losing nephrons and reach 50% you damage the remaining and progress to renal failure

8
Q

Define Nephrotic Syndrome

A

Loss of glomeruli –> Can’t filter –> Lose protein

9
Q

3 Blood/urine findings of Nephrotic

1 physical finding

A

Proteinuria > 3.5/day
Hypoalbuminemia <3 gram
Lipidemia

Edema due to low albumin

10
Q

Number systemic disease cause of nephrotic syndrome?

A

Diabetes mellitus

11
Q

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.

A

Minimal Change Disease

12
Q

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

A

Membranous Nephropathy

13
Q

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.

A

FSGS

14
Q

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.

A

Type 1 Membranoproliferative Glomerulonephritis

15
Q

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.

A

Type 2 Membranoproliferative Glomerulonephritis

16
Q

4 Findings of Nephritic Syndromes

A
  1. Hematuria
  2. Oliguria
  3. Azotemia
  4. HTN
17
Q

3 Morphological signs of Nephritic syndromes

A
  1. Proliferation of glomerular cells
  2. Inflammatory cells in glomerulus
  3. RBC casts in urine
18
Q

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.

A

Post Streptococcal GN

19
Q

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.

A

Type 1 RPGN with Goodpasture’s

20
Q

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.

A

Type 2 RPGN

21
Q

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

A

Type 3 RPGN

22
Q

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.

A

IgA Disease/Berger’s Disease

23
Q

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.

A

Alport Syndrome/Hereditary Nephritis

24
Q

Patient presents with hematuria but recovers quickly. Patient has heterozygous genotype for abnormality in type IV collagen.

A

Benign Familial Hematuria/ Thin Basement Membrane Disease

25
Q

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.

A

SLE Nephropathy

26
Q

This is the #1 cause of end stage renal disease in US

A

Diabetic Associated Renal Disease

27
Q

This is the #1 cause overall for nephrotic syndrome in adults in US.

A

Diabetic Associated Renal Disease

28
Q

Patient presents with Nodular glomerulosclerosis with Kimmelstiel-Wilson nodules on staining.

A

Glomerular Disease of Diabetic Associated Renal Disease

29
Q

Patient presents with hyaline arteriolosclerosis.

A

Renal Arteriolosclerosis of Diabetic Associated Renal Disease

30
Q

Patient presents with increased infections from glycosuria, bladder stasis, and altered immune status.

A

Pyelonephritis of Diabetic Associated Renal Disease

31
Q

This is the most common cause of papillary necrosis

A

Diabetes

32
Q

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.

A

Amyloidosis

33
Q

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.

A

Light Chain Deposition Disease

34
Q

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.

A

Light Chain Cast Nephropathy

35
Q

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.

A

Cryoglobulinemic Nephritis

36
Q

Patient presents with nephrotic syndrome that looks like amyloid but does not stain amyloid.

A

Fibrillary Immunotactoid glomerulonephritis

37
Q

African-American presents with FSGS of the collapsing variant.

A

HIV nephropathy

38
Q

Patient rejects a kidney transplant on the operating table.

A

Hyperacute Rejection

39
Q

Patient rejects a kidney transplant due to preformed antibodies against the graft.

A

Hyperacute Rejection

40
Q

Patient has CD8 cytotoxic T cells attack the endothelial cells of his or her kidney transplant.

A

Acute - Cellular

41
Q

Patient has rejection vasculitis months after transplant of new kidney.

A

Acute - Humoral

42
Q

Patient presents with a slow steady increase in serum creatinine while slowly losing renal function.

A

Chronic

43
Q

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.

A

Polyoma Virus (BK)

44
Q

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

A

Pre-Renal ARF

Hydration/Volume expansion

45
Q

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

A

Renal ARF

Supportive (NOT HYDRATION)

46
Q

Patient presents with rapid decline in renal function over 24 hours. A surgical operation cures the problem.

A

Post-Renal ARF.

47
Q

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.

A

Chronic Renal Failure

48
Q

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.

A

Acute Tubular Necrosis