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Question 1

Although there are numerous disease states and conditions which can lead to altered kidney function, there are relatively few renal syndromes. Any condition affecting the function of the kidney should address the following questions:

Answer 1

Does this represent an acute or chronic process?2) Is this pre-renal, intrinsic, or post-renal in origin?3) If, intrinsic, Is the process primarily glomerular, tubular, or vascular in origin?4) Is the process inflammatory or non-inflammatory?5) Is the process associated with an underlying systemic disease?

Question 2

What are the glomerular syndromes?

Answer 2

-nephrotic syndrome-nephritic syndrome (rapidly progressive glomerulonephritis is the most severe form of the nephritic syndrome)-mesangial nephritic pattern-mixed nephritic -nephrotic syndrome-chronic glomerular disease

Question 3

What are the tubular syndromes?

Answer 3

-Non-inflammatory tubular interstitial disease-inflammatory tubular interstitial disease (e.g., allergic interstitial nephritis)-acute pyelonephritis-chronic interstitial disease

Question 4

What are the vascular syndromes?

Answer 4

-prerenal azotemia (reduced renal blood flow or reduced renal perfusion pressure)-renal artery stenosis (unilateral or bilateral)-hypertensive nephrosclerosis (ischemic nephropathy)-vasculitis (typically presents as nephritic syndrome)

Question 5

Classic presentation of nephrotic syndrome?

Answer 5

-3+ proteinuria-edema-hypoalbuminuria-protein/cr ratio high-lipiduria

Question 6

T or F. Patients with pure nephrotic syndrome typically have normal glomerular filtration rate, normal blood pressure, normal acid-base status.

Answer 6

T.

Question 7

Why does edema occur with nephrotic syndrome?

Answer 7

The edema is a consequence of avid sodium retention by the kidney as a result of enhanced renal tubular sodium reabsorption (particularly in the distal portions of the nephron). The retained salt and water is primarily restricted to extracellular fluid volume. Because of decreased plasma oncotic pressure (due to albuminuria), there is a disproportionate increase in the size of the interstitial fluid volume.

Question 8

The plasma volume remains normal until there is profound hypoalbuminemia (less than 2g/dl)

Answer 8

You see loss of albumin which promotes interstitial fluid movement which would decrease plasma volume but at the same time you see increased Na and water reabsorption to the ECF

Question 9

Is pulmonary edema a feature of nephrotic syndrome. Why or why not?

Answer 9

No, since intravascular volume remains normal, pulmonary edema is not a feature of nephrotic syndrome.

Question 10

What may be seen in urinalysis with nephrotic syndrome?

Answer 10

There may be oval fat bodies and fatty casts related to lipiduria.

Question 11

What is the most common intrinsic glomerular disease leading to nephrotic syndrome in Caucasian adults?

Answer 11

Membranous glomerulopathy

Question 12

What is the most common cause of nephrotic syndrome in African-American adults? Second most common?

Answer 12

focal segmental glomerulosclerosis and second leading cause in this population is membranous glomerulopathy

Question 13

The overall most common cause of nephrotic syndrome in adults is what?

Answer 13

diabetic nephropathy

Question 14

Describe diabetic nephropathy

Answer 14

A slowly developing noninflammatory process which is first clinically detected by the presence of microalbuminuria and later with overt proteinuria, frequently leading to nephrotic syndrome. By the time heavy proteinuria is present there is also decreasing glomerular filtration rate.

Question 15

What does diabetic nephropathy progress to?

Answer 15

chronic renal insufficiency and ultimately ERSD. Diabetic nephropathy is the most common etiology for end-stage renal disease in the United States.

Question 16

How is nephritic syndrome described?

Answer 16

The presence of inflammatory changes within the glomerulus. Inflammatory changes are often accompanied by pro inflammatory cytokines and mediators, complement activation, proliferation of mesangial cells, infiltration of glomerulus by inflammatory cells (mononuclear and PMN’s), endothelial cell swelling. The net result of these histologic changes is decreased surface area for glomerular filtration, leading to decreased GFR.

Question 17

Inflammation in nephritic syndrome leads to what?

Answer 17

Inflammation predictably leads to glomerular hematuria. Red cells excreted into the urine are often crenated and dysmorphic in appearance

Question 18

How are red cell casts made in nephritic syndrome?

Answer 18

Red blood cells may become incorporated into the Tamm Horsfall protein matrix in the tubular lumen producing red blood cell casts. Red blood cell casts are pathognomonic for intense glomerular inflammation

Question 19

There may also be abnormal permeability of the glomerular capillary wall to protein in nephritic syndrome. So why isn’t there as much proteinuria?

Answer 19

The concomitant decreased GFR leads to less quantitative proteinuria. The level of protein excretion is generally less than 2g per day, corresponding to spot urine protein creatinine ratio of approximately ~2, and urinary dipstick approximately 2+ or less for protein

Question 20

Nephritic syndrome is more likely to present with pulmonary edema. Why?

Answer 20

Since there is less albuminuria, serum albumin concentration and plasma oncotic pressure remain near normal. The decreased GFR and changes in Starling’s forces in peritubular capillaries lead to avid salt and water retention. Given the normal plasma oncotic pressure, this means there is considerable increase in both the plasma volume and interstitial fluid volume. Increased blood volume will be manifest as hypertension and pulmonary congestion, in addition to interstitial edema. Thus, these patients can present with pulmonary edema. Increased interstitial fluid volume leads to peripheral edema.

Question 21

What is the prototype of nephritic syndrome?

Answer 21

PIGN

Question 22

Some forms of glomerulonephritis lead to inflammatory changes which are restricted to the mesangial area of the glomerulus. What is the result?

Answer 22

This leaves the remainder of the glomerular capillary loop unaffected.

Question 23

Is GFR preserved in mesangial nephritic syndromes?

Answer 23

Since the glomerular capillary wall is relatively well preserved, GFR is typically normal and there is minimal proteinuria.

Question 24

Is hematuria a symptom of mesangial nephritic syndromes?

Answer 24

Yes, which can be either microscopic or macroscopic. Red blood cell casts may be present.

Question 25

Do mesangial nephritic syndromes present with signs of volume overload?

Answer 25

No, since GFR is preserved and there is minimal proteinuria, there is typically no evidence for volume expansion, HTN, or edema formation.

Question 26

What is a classic example of mesangial nephritic syndrome?

Answer 26

IgA nephropathy The IgA immune deposits are restricted to the mesangium. SLE may also be associated with immune deposits restricted to the mesangium.

Question 27

Some diseases have features of both nephritic and nephrotic syndromes. There will be evidence for inflammatory glomerular disease, such as hematuria, red blood cell casts, and worsening GFR. In addition there is nephrotic range proteinuria often leading to hypoalbuminemia and edema. What are some examples?

Answer 27

SLE, diffuse proliferative form is the prototype. Other examples include membranoproliferative glomerulonephritis (idiopathic forms and secondary forms, such as hepatitis C related)

Question 28

Chronic glomerular disease is typically recognized by the presence of abnormal urinalysis and abnormal GFR (increased serum creatinine conc. ,ie, chronic kidney disease).

Answer 28

Chronic kidney disease is due to a decreased number of functioning nephrons, and tends to be inexorably progressive.

Question 29

T or F. Chronic renal insufficiency frequently leads to decreased size kidneys.

Answer 29

T.

Question 30

What are some urinary findings unique to chronic renal insufficiency?

Answer 30

Waxy casts, seen in any form of chronic renal insufficiency. They are not helpful in determining etiology of the renal disease. Waxy casts simply denote chronicity

Question 31

Why does tubulointerstitial disease decrease GFR?

Answer 31

In this setting, tubules and renal interstitium have been damaged by noninflammatory mechanisms. Damaged tubules have impaired ability to reabsorb glomerular filtrate, leading to the increased intra-tubular pressures. This dissipates the hydrostatic pressure gradient between the glomerular capillary and the renal tubule and therefore decreases glomerular filtration. In short, when the renal tubule fails to reabsorb, glomerular filtration decreases, even though the glomerulus is histologically intact.

Question 32

What are the clinical manifestations of noninflammatory tubulointerstitial disease?

Answer 32

acute decrease in GFR, leading to increased serum creatinine concentrations. Urinalysis findings: there will be minimal proteinuria, since glomeruli are normal. There is frequently minimal or absent hematuria.

Question 33

What will be the urine SG in non-inflammatory tubulointerstitial disease?

Answer 33

Urinary specific gravity is typically 1.010, corresponding to urine osmolality of ~ 300mosm/kg, which is similar to plasma osmolality. This is known as isosthenuric urine.

Question 34

Why do you see isosthenuric urine in tubulointerstitial disease?

Answer 34

The damaged renal tubule can neither concentrate nor dilute the urine, thus, urine osmolality is the same as the initial glomerular filtrate which always has the same osmolality as plasma.

Question 35

What are the urinary sediment abnormalities seen in Noninflammatory tubulointerstitial disease?

Answer 35

granular casts are the hallmark feature.

Question 36

What causes granular casts?

Answer 36

The granular material represents fragments of cellular debris from injured cells. There may also be sloughed renal tubular epithelial cells. These may become incorporated into casts, renal tubular cell casts.

Question 37

T or F. There are no inflammatory cells in noninflammatory tubulointerstitial disease

Answer 37

T. The absence of inflammatory response is suggested by the relative absence of inflammatory cells (wbc) and red blood cells in the urinary sediment.

Question 38

What are some examples of Noninflammatory tubulointerstitial disease?

Answer 38

acute tubular necrosis is the prototype. Direct renal tubular nephrotoxic agents

Question 39

What causes ATN?

Answer 39

Renal tubules are damaged by prolonged ischemia. Oxygen consumption by the kidney occurs primarily in the renal tubules, thus they are most susceptible to ischemic injury.

Question 40

What are some directly nephrotoxic drugs that cause noninflammatory tubulointerstitial damage?

Answer 40

Aminoglycosides, Ampho B, heavy metals, cisplatin, intravenous contrast media, cyclosporine, tacrolimus, lithium, myoglobin, free hemoglobin.

Question 41

The inflammatory cells in inflammatory tubulointerstitial disease are frequently _______.

Answer 41

mononuclear cells, but may also include eosinophils and neutrophils.

Question 42

Can you differentiate non-inflammatory from inflammatory tubulointerstitial disease by urinary SG, Uosm, or dipstick?

Answer 42

No, the urinary specific gravity, urine osmolality, and urinary dipstick changes are similar to those in non-inflammatory tubular diseases.

Question 43

So how can you differentiate between non-inflammatory from inflammatory tubulointerstitial disease?

Answer 43

Additional findings, however, may include positive leukocyte esterase, when urinary neutrophils are present, and microscopic hematuria

Question 44

What are some examples of inflammatory tubulointerstitial disease?

Answer 44

acute kidney transplant rejection is the prototype. -allergic interstitial nephritis

Question 45

What happens in acute kidney transplant rejection?

Answer 45

The allograft is recognized as foreign antigen and an immune response is directed against the renal tubular cells which express histocompatibility antigens.

Question 46

What typically causes allergic interstitial nephritis?

Answer 46

medications or viral infections in an idiosyncratic manner

Question 47

How do meds or viral infections cause AIN?

Answer 47

The viral or drug antigens act as haptens, leading to an inflammatory immune response directed against renal tubules. Since this is an allergic response, some of the infiltrating cells are eosinophils, frequently leading to the presence of eosinophils in the urine.

Question 48

How are urinary eosinophils detected?

Answer 48

By Hansel’s stain or by Wright’s stain.

Question 49

Most of the urinary white blood cells in inflammatory tubulointerstitial injury are what?

Answer 49

neutrophils (with some eosinophils). This represents sterile pyuria (absence of bacteria)

Question 50

What drugs can cause AIN?

Answer 50

-Dilantin, -allopurinol, -beta-lactam antibiotics, -sulfa derivative -antibiotics, -cimetidine.

Question 51

Describe acute pyelonephritis

Answer 51

Acute bacterial infection leading to inflammatory tubular injury: ascending bacterial infection leading to bacterial infection and neutrophil inflammatory response in the medulla. Typically unilateral, leading to decreased function of the affected kidney. Untreated, it can lead to urosepsis and destruction of renal parenchyma.

Question 52

How does acute pyelonephritis present upon urinalysis?

Answer 52

-leukocyte esterase positive, -frequently nitrite positive, -frequently positive for blood (blood is from the urinary tract rather than kidney).

Question 53

How does acute pyelonephritis present upon urine sediment exam?

Answer 53

Marked pyuria, white blood cell clumps, and bacteria. There may be white blood cell casts.

Question 54

How does obstructive uropathy present?

Answer 54

Obstructed tubules cannot perform normal tubular function such that isosthenuric urine will be formed and fractional excretion of sodium typically will be > 1%.

Question 55

Urinary findings of obstructive uropathy:

Answer 55

Variable degree of hematuria (red blood cells will be coming from the urinary tract rather than kidney). In the absence of infection there will be no evidence of inflammation,ie, minimal pyuria.