Renal Flashcards
(110 cards)
0
Q
New bicarbonate is generated by secretion of protons into urinary buffers (phosphate and ammonia) that are then eliminated. Proton secretion is stimulated by ___________ (2). Bicarbonate reabsorption is stimulated by ____________ (3). The renal response to changes in extracellular pH is slower than the respiratory response, generally requiring ________ hours for a maximal response.
A
acidosis and aldosterone secretion
hypercapnia, extracellular volume contraction, and severe potassium depletion
24 to 48
1
Q
For each Type of Stone: Urine pH, type of Crystals, findings on Radiograph: Calcium (oxalate) Uric acid Struvite Cystine
A
Type of Stone - Urine pH (N 5.5 to 6.0) - Crystals - On Radiograph
Calcium (oxalate) - Increased - dumbbell or envelope - Radiopaque
Uric acid - Decreased - Rhomboid - RadioLUCENT
Struvite - Increased - Coffin lid - Radiopaque (= magnesium ammonium phosphate; more common in women due to assoc with UTIs/urease-prod bacteria such as Proteus)
Cystine - Decreased - Hexagonal - Radiopaque (assoc with cystinuria = inherited defect of AA transport)
2
Q
Normal serum anion gap
A
8 to 12 mEq per L
3
Q
Reclamation of HCO3- is driven by ___________ in the proximal tubule and by ___________ in the distal tubule.
Regeneration of HCO3- occurs mainly in the _________ tubule. This results in the net secretion of hydrogen ion into the tubule, where it combines with _________(2) and is eliminated from the body.
A
Na/H exchange; the proton pump
distal; phosphate and ammonia
4
Q
Expected compensation in Metabolic acidosis
A
1.0 to 1.5 mm Hg fall in PaCO2 for each 1 mEq per L decrease in HCO3- (maximal decrease is to PaCO2 12 to 15 mm Hg)
5
Q
Expected compensation in Metabolic alkalosis
A
0.25 to 1.0 mm Hg rise in PaCO2 for each 1 mEq per L rise in HCO3-
6
Q
Expected compensation in Respiratory acidosis
A
Acute, 0.1 mEq per L rise in HCO3- for each 1 mm Hg of PaCO2 rise over 40 mm Hg
Chronic, 0.3 mEq per L rise in HCO3- for each 1 mm Hg of PaCO2 rise over 40 mm Hg
7
Q
Expected compensation in Respiratory alkalosis
A
Acute, 0.1 to 0.3 mEq per L fall in HCO3- for each 1 mm Hg of PaCO2 decrease below 40 mm Hg
Chronic, 0.2 to 0.5 mEq per L fall in HCO3- for each 1 mm Hg of PaCO2 decrease below 40 mm Hg
8
Q
Causes of metabolic acidosis With increased anion gap: (4)
A
Lactic acidosis (from inadequate tissue oxygenation, hepatic failure, neoplasms) Ketoacidosis (from diabetes, starvation, alcoholism) Poisons/drugs (salicylates, methanol, ethylene glycol) Renal failure (chronic, end-stage disease)
9
Q
Causes of metabolic acidosis With normal anion gap: (3)
A
Renal tubular disorders (renal tubular acidosis, potassium-sparing diuretics, hypoaldosteronism)
Loss of base (diarrhea, carbonic anhydrase inhibitors, ureterosigmoidoscopy, pancreatic fistula)
Excess acid intake (ammonium chloride, cationic amino acids)
10
Q
Causes of metabolic alkalosis (4)
A
Volume loss with chloride depletion (vomiting, gastric drainage, diuretics, villous adenoma) Hypermineralocorticoid states (exogenous steroid treatment, primary aldosteronism, Cushing syndrome, renovascular disease) Severe potassium deficiency Excess alkali intake (milk-alkali syndrome, bicarbonate administration)
11
Q
Causes of respiratory acidosis (2) and alkalosis (4)
A
CAUSES OF RESPIRATORY ACIDOSIS
Acute respiratory failure (drug intoxication, cardiopulmonary arrest)
Chronic respiratory failure (chronic obstructive pulmonary disease [COPD], neuromuscular disorders, obesity)
CAUSES OF RESPIRATORY ALKALOSIS
Hypoxia stimulating hyperventilation (asthma, pulmonary edema, pulmonary fibrosis, high altitude, congenital heart disease)
Increased respiratory drive (pulmonary disease, anxiety, salicylate intoxication, cerebral disease, fever)
Cirrhosis, pregnancy
Excessive mechanical ventilation
12
Q
Sign/symptom in:
- acute metabolic acidosis (1)
- acute respiratory acidosis (1)
- acute respiratory alkalosis (1)
A
- acute metabolic acidosis: Profound hyperventilation (Kussmaul respiration)
- acute respiratory acidosis: Papilledema with severe, acute hypercapnia
- acute respiratory alkalosis: Neurologic symptoms (paresthesias, numbness, light-headedness)
13
Q
Technical aspects that can affect the accuracy of ABGs/electrolytes: (5)
A
- Delay in processing the sample or not keeping the sample on ice
- Contamination of the sample with excess heparin
- Failure to purge air from the syringe
- A difficult arterial puncture leading to a respiratory alkalosis caused by pain and anxiety
- Sampling of venous blood instead of arterial blood: can result in severe misreadings (usually decreased pH and PO2 and increased PCO2), particularly in disease states that impair peripheral oxygen delivery and/or increase peripheral metabolism.
14
Q
Generally, if the underlying disturbance is corrected, the kidneys and lungs restore acid-base balance; however, several conditions may require specific therapeutic interventions; what are they in each case?
- metabolic acidosis in the setting of chronic renal failure
- severe uncorrectable metabolic acidosis in the setting of acute renal failure
- metabolic alkalosis from volume and chloride loss
A
- metabolic acidosis in the setting of chronic renal failure (administration of oral bicarbonate)
- severe uncorrectable metabolic acidosis in the setting of acute renal failure (temporary hemodialysis)
- metabolic alkalosis from volume and chloride loss (fluid replacement with saline solution).
15
Q
The plasma sodium concentration reflects both ________ and ________.
A
extracellular fluid osmolality and total body water
16
Q
Treatment of hyponatremia or hypernatremia requires ___________.
A
assessment of the patient’s volume status
17
Q
When treating free water deficit in hypernatremia, a maximum of _________ should be replaced in the first _____ hours.
A
half the water deficit; 24
18
Q
Potassium levels over 6 may result in which 2 ECG findings? Why must patient be monitored closely?
A
peaked T waves and diminished R waves
Require close monitoring for cardiac arrhythmias.
19
Q
Water constitutes approximately _______% of body weight. Approximately ______% of total body water (TBW) is intracellular fluid (ICF), and ________% is extracellular fluid (ECF). The plasma volume constitutes approximately ______% of the ECF, and the remaining ____% is interstitial fluid.
A
50% to 60%
two thirds; one third
25%; 75%
20
Q
All principal electrolytes in the body are asymmetrically distributed across cell membranes. ________ is the principal extracellular cation, with _________ and ___________ the main extracellular anions. _____________ (4) are the main intracellular electrolytes.
A
Sodium, chloride, bicarb
Potassium, calcium, magnesium, and organic anions (e.g., proteins)
21
Q
____________ generally reflects the osmolality of the ECF.
A
the plasma sodium concentration (because sodium salts account for more than 90% of the osmolality of the ECF)
22
Q
Location of peripheral receptors that sense the effective blood volume (3). These receptors regulate renal sodium handling via ________. (2)
A
atria, central arteries, and juxtaglomerular apparatus
the renin-angiotensin system and a number of natriuretic hormones
23
Q
Plasma osmolality is regulated via the action of ___________, which is produced in response to _________. What are its actions on the kidney?
A
antidiuretic hormone (ADH), which is produced by the hypothalamus in response to increased plasma osmolality
ADH acts on the kidney to reduce urine volume and increase urine osmolality, thus conserving water. Similarly, in the absence of ADH, the kidneys produce very dilute urine.
24
A pure excess of sodium results in _________ (1), as seen in _________ (3).
Edema; heart failure, cirrhosis, and the nephrotic syndrome
25
Hyponatremia correction in: (1) severe volume depletion, (2) edematous states?
Unless severe neurologic symptoms are present, correction should be at a rate of approximately __________. Care must be taken not to raise the plasma sodium level too rapidly because it can cause _________.
Severe volume depletion: IV normal saline (0.9%) (hypertonic saline is almost never required). Edematous states: free water restriction.
```
8 to 12 mEq/L/24 hours.
neurologic damage (central pontine myelinolysis)
```
26
Sustained hypernatremia usually only occurs in which patients?
Hypernatremia results from a deficit in water relative to solute. Hypernatremia invariably results in hyperosmolarity. This in turn normally results in ADH secretion that stimulates renal water conservation and thirst. Therefore, sustained hypernatremia usually only occurs in patients who are unable to respond to thirst by drinking (e.g., young children and mentally and/or physically limited adults).
27
Hypernatremia correction involves which fluids? How to calculate free water deficit? How quickly should correction be done?
oral or IV replacement of water as well as sodium replacement if required.
FWD = 0.6 × body weight (kg) × ([Na]serum/140) - 1)
Only half of the free water deficit should be replaced in the first 24 hours, and the remainder of the deficit over the next 24 to 48 hours.
28
___________ is the principal determinant of membrane excitability in nerve and muscle cells.
The ratio of intracellular to extracellular potassium
29
____________ stimulates renal potassium excretion.
Balance between intracellular and extracellular potassium is influenced by ___________ (2). How does each factor influence this balance?
Aldosterone
(1) Acid-base balance, with acidosis favoring a shift of potassium out of cells. (2) Hormones: Insulin and β-adrenergic catecholamines promote the movement of potassium into cells.
30
Potassium depletion results from insufficient dietary potassium intake or increased loss. Potassium loss can occur via: (8)
GI loss (diarrhea, vomiting, villous adenoma, ureterosigmoidostomy)
Diuretic use
Metabolic alkalosis (renal wasting because of bicarbonate excess)
Mineralocorticoid excess
Licorice intoxication (caused by a compound with mineralocorticoid-like activity)
Glucocorticoid excess
Renal tubular disease (renal tubular acidosis, certain antibiotics)
Shift of potassium into the intracellular compartment (from insulin effect, alkalosis) can result in hypokalemia without an actual total body potassium deficit
31
4 tissues/organs where manifestations of hypokalemia are seen; what are the manifestations?
(disturbances in the function of excitable tissues:)
```
Skeletal muscle (weakness, particularly of the lower extremities; rhabdomyolysis)
Smooth muscle (GI ileus)
Cardiac muscle (prominent U waves on electrocardiogram; cardiac arrest, with rapid reduction of serum potassium, enhanced digitalis toxicity)
Peripheral nerves (decreased or absent tendon reflexes)
```
32
Potassium replacement in hypokalemia: what is used in less severe cases? In more severe cases, what are appropriate concentrations and rates of correction?
- generally done via oral supplementation (potassium chloride) - slower and safer
- severe hypokalemia or hypokalemia in patients who cannot absorb oral supplements: IV potassium solutions should normally contain at most 60 mEq per L and should be administered no faster than 20 mEq per hour to avoid cardiac toxicity from transient hyperkalemia.
33
Hyperkalemia can occur via a number of mechanisms: (6)
Inadequate renal excretion (acute renal failure, end-stage renal failure, tubular disorders)
Adrenal insufficiency
Administration of potassium-sparing diuretics (spironolactone, amiloride)
Tissue damage with release of intracellular potassium (muscle crush injury, hemolysis, internal hemorrhage)
Shift of potassium from the intracellular compartment (acidosis, insulin deficiency, digitalis poisoning, β-adrenergic antagonists)
Excess potassium intake (usually in the setting of underlying renal insufficiency)
Note: in most cases, significant hyperkalemia, regardless of underlying cause, generally has a component of decreased or impaired renal potassium excretion because the kidneys can usually rapidly excrete an excess of potassium present in the serum.
34
The major toxicity of hyperkalemia is ___________. Electrocardiogram (ECG) manifestations of hyperkalemia include: (6, in order; 2 additional signs)
the development of cardiac arrhythmias
```
1 Peaking of T waves (earliest sign)
2 Diminished R waves
3 QRS widening
4 PR prolongation
5 Loss of P wave (Atrial asystole)
6 Sine wave
```
Also:
Complete heart block
Ventricular fibrillation/standstill
35
Why isn't the absolute serum potassium level a very good indicator of patients who have a life-threatening potassium overload?
Because the serum potassium represents only a small fraction of the total body potassium load, small changes in serum levels can indicate a significant change in total body potassium. Therefore, the absolute serum potassium level is not a very good indicator of patients who have a life-threatening potassium overload. However, any patient who presents with a potassium level >6.0 mEq per L should be monitored carefully for the development of cardiac arrhythmias.
36
Tx of hyperkalemia: 3 groups of therapies
```
Antagonize the toxic effects of excess potassium on excitable membranes (Membrane stabilization):
Calcium administration (does not lower plasma potassium levels but counteracts the effect of hyperkalemia on excitable membranes—transient effect)
```
Immediately lower the serum potassium (Intracellular shift of potassium):
Insulin administration (with concomitant glucose administration to avoid hypoglycemia)
IV bicarbonate
Elimination of excess potassium (slower than the prev 2 groups; use the 1st 2 strategies first in an emergency):
Use of oral potassium-binding resins to promote GI removal of potassium
Diuretics and saline infusion
Dialysis (hemodialysis and peritoneal—generally in several renal impairments)
37
How do the kidneys regulate blood pressure? (2)
via secretion of renin and prostaglandins
38
Acute renal failure (ARF) occurs over what time frame?
hours to days
39
Prerenal ARF etiologies (6 categories):
Hypovolemia (e.g., from blood loss, dehydration)
Decreased cardiac output (e.g., during acute myocardial infarction, cardiac arrest)
Renovascular disease (e.g., dissection of renal artery, renal artery thrombosis)
Systemic vasodilation (e.g., from administration of systemic vasodilator agents)
Renal vasoconstriction (e.g., from administration of vasopressor agents)
Impairment of renal autoregulation of blood flow (e.g., caused by drugs such as angiotensin-converting enzyme [ACE] inhibitors or nonsteroidal anti-inflammatory drugs).
40
Intrinsic renal ARF etiologies (5):
Vasculitis or microangiopathy
Glomerulonephritis
Acute tubular necrosis (can be caused by an ischemic insult or nephrotoxic drugs such as aminoglycoside antibiotics or radiographic contrast agents)
Interstitial nephritis (often an allergic-type reaction to various drugs such as β-lactam antibiotics)
Tubular obstruction
41
Postrenal ARF etiologies (3):
```
Ureteral obstruction (e.g., because of tumor, retroperitoneal hemorrhage, or nephrolithiasis)
Bladder neck obstruction (e.g., because of tumor)
Urethral obstruction (e.g., secondary to an enlarged prostate, bladder thrombus, or renal calculus)
```
42
ARF is more commonly encountered in the hospital setting (occurring in up to ______% of all hospitalized patients), where it is associated with: (6)
5%
Surgery
Trauma (hemorrhage, muscle injury)
Administration of nephrotoxic drugs (aminoglycoside antibiotics, contrast agents)
Bladder catheterization
Sepsis
Shock (low cardiac output states and the use of vasoactive drugs)
43
Complications and symptoms of ARF commonly seen are: (5)
Intravascular volume overload (dyspnea, orthopnea, edema)
Metabolic acidosis (dyspnea)
Anemia (fatigue)
Hyperkalemia
Uremic syndrome (when BUN is over 60 to 100 mg/dL: anorexia, nausea/vomiting, pruritus, mental status changes, serositis/pericarditis, coagulopathy)
44
The uremic syndrome is a constellation of symptoms and physical findings that result from the accumulation of toxins normally handled by the kidney: (4)
Pericarditis (manifested by a cardiac rub)
Uremic frost (crystals of urea that collect on the skin)
Asterixis
Uremic fetor (a urine-like odor to the breath because of accumulating nitrogenous waste products)
45
Analysis of urine sediment in ARF can provide important information:
The presence of red blood cells (RBCs), either alone or in casts suggests _____________.
White blood cells (WBCs) and white cell casts are seen in __________. Granular casts (in particular, “muddybrown” casts) are often seen in __________ but are generally less specific than the other types of casts.
Assessment of the degree of proteinuria by a 24-hour urine collection can give clues to the etiology:
Generally, nephrotic-range proteinuria (i.e., more than 3 g per 24 hours) indicates __________. Lesser amounts are usually seen in __________.
glomerular or vascular lesions
interstitial nephritis
acute tubular necrosis
a glomerular lesion
interstitial disorders
46
Formula for fractional excretion of sodium (FENa)?
| What is it used for and how to interpret it? What other lab measurement is used in conjunction to confirm this?
FENa = 100 × (urine Na/serum Na ÷ urine Cr/serum Cr)
-can be used to distinguish prerenal azotemia from other etiologies
-In prerenal, FENa 500 mOsm/kg H2O) supports the diagnosis of prerenal failure due to a stimulus to preserve intravascular volume through water retention.
If volume deficiency prerenal conditions are suspected, a fluid challenge may be considered both diagnostically and therapeutically.
47
If ARF due to a glomerular process is suspected from the clinical context, what lab tests should be done? (5)
immune-mediated disease can be screened for by measurement of antinuclear antibodies, antineutrophil cytoplasmic antibodies (antineutrophil cytoplasmic antibodies [ANCAs]; seen in Wegener granulomatosis), antiglomerular basement membrane (anti-GBM) antibodies, complement levels, and cryoglobulins.
48
The nuclear medicine renal scan can detect ___________ but is less sensitive in detecting ________.
unilateral renal artery stenosis; bilateral renal artery disease
49
When to do kidney biopsy to Dx ARF?
The use of renal biopsy has decreased in recent years. Traditionally used in the diagnosis of glomerulopathies, the development of serologic tests such as ANCA and antiGBM has allowed many diagnoses to be made without biopsy. However, in cases where the diagnosis is uncertain, consultation of a nephrologist with possible biopsy can be useful in making a diagnosis or in giving prognostic information.
50
During the management of ARF, avoid which drugs (if possible)? (2 classes)
Drugs that are nephrotoxic (such as radiocontrast dye or certain antibiotics)
Drugs that reduce renal blood flow (such as NSAIDs)
51
In prerenal failure secondary to absolute hypovolemia, replacement of fluid depends on the mechanism of loss. Fluid deficit because of hemorrhage should be corrected with ________ (2). GI fluid loss is generally ___________ (hyper-/hypotonic) and should be replaced accordingly.
saline and red cells
| hypotonic
52
Tx for acute tubular necrosis?
In many cases of acute tubular necrosis, which is often caused by nephrotoxic agents, once the offending agent is removed, renal function will often return and supportive measures are all that is necessary.
53
Conditions leading to CKD and % for each: (5)
```
Diabetes (>50% of cases)
Hypertension (20% to 30% of cases)
Glomerulonephritis (10%)
Interstitial nephritis (3%)
Polycystic kidney disease (3%)
```
54
Uremia refers to the syndrome resulting from the failure of the kidneys to perform their normal excretory, metabolic, and endocrine functions. Uremia is a complex syndrome that includes a variety of physiologic and clinical abnormalities: (7 categories)
Fluid and electrolyte abnormalities: fluid overload, metabolic acidosis, sodium imbalances, hyperkalemia, hyperphosphatemia, hypocalcemia
Endocrine/metabolic abnormalities: hypertriglyceridemia, vitamin D deficiency, secondary hyperparathyroidism, osteodystrophy, hyperuricemia, impotence
Cardiovascular disorders: hypertension, heart failure, pericarditis, accelerated atherosclerosis
GI disturbances: anorexia, nausea/vomiting, peritonitis, ascites, hemorrhagic colitis
Dermatologic abnormalities: pruritus, uremic frost, hyperpigmentation
Hematologic/immunologic abnormalities: anemia (generally normochromic, normocytic), impaired platelet function, leukopenia, T-cell dysfunction (leading to increased risk of infection)
Neurologic/neuromuscular abnormalities: fatigue, asterixis, headache, myoclonus, seizures, peripheral neuropathy, altered mentation, coma
55
__________ is the most common cause of death in patients with CKD.
cardiovascular disease
56
At approximately _______% of normal GFR, biochemical evidence of renal failure can be seen, but patients are generally asymptomatic. Symptoms generally do not appear until renal function (as measured by GFR) declines to _______% of normal.
30% to 40%
| 10% to 15%
57
The history and physical examination findings in a patient with advanced CKD are manifestations of the abnormalities associated with uremia: (5 categories)
Fatigue, shortness of breath, pruritus, headache
Peripheral edema, ascites
Auscultatory rales, pericardial rub
Bruising, uremic frost, hyperpigmentation
Asterixis, peripheral neuropathy, and altered mental status
58
GFR can be estimated in a number of ways. (3)
24-hour urine collection (creatinine clearance = urine Cr × volume/plasma Cr),
More commonly: estimate based on the plasma creatinine level using the Cockcroft-Gault equation or the Modification of Diet in Renal Disease (MDRD) study equation. Both of these formulas are not accurate in the setting of rapidly changing renal function.
59
Peritoneal dialysis: what is the most common type? What are 2 issues with this method?
Most common method: continuous ambulatory peritoneal dialysis (CAPD), involves having the patient continually carry approximately 2 L of dialysis fluid in the peritoneal cavity. The fluid is then exchanged four times a day. Because exchange is accomplished by gravity flow, no machinery is required and dialysis can be performed virtually anywhere. Issues: compliance, peritonitis.
60
Monitoring of CKD involves _________. (2)
Monitoring of CKD involves serial calculation of estimated GFR (based on the plasma creatinine) and monitoring for the development of proteinuria.
61
Diet modification is a key element in the conservative treatment of CKD - what does it involve? (3)
(1) Restriction of fluid and sodium can diminish secondary hypertension. In some cases, diuretics may be required. At the same time, dehydration must be avoided to prevent prerenal azotemia.
(2) As renal function declines further, restriction of dietary phosphate and potassium becomes necessary.
(3) Protein reduction can relieve uremic symptoms and delay progression of renal failure. Dietary protein intake of 0.55 to 0.6 g/kg/day is sufficient to prevent negative nitrogen balance while relieving uremia.
62
Chronic kidney disease definition?
| End-stage renal disease (kidney failure) definition?
Chronic kidney disease definition:
Kidney damage for ≥3 mo based on findings of abnormal structure (imaging studies) or abnormal function (blood tests, urinalysis)
or
GFR below 60 mL/min/1.73 m2 for ≥3 mo with or without evidence of kidney damage
End-stage renal disease (kidney failure) definition:
GFR below 15 mL/min/1.73 m2
or
Need for kidney replacement therapy (dialysis or transplant)
63
Stages of Chronic Kidney Disease Based on Estimated GFR
```
Stage - GFR (mL/min/1.73 m2)
I ≥90
II 60 to 89
III 30 to 59
IV 15 to 29
V less than 15 or dialysis
```
64
The glomerulopathies are a heterogeneous group of disorders characterized by direct injury to the glomerulus, as opposed to other intrinsic renal pathologies such as tubulointerstitial diseases or primary vascular diseases. Because the glomerulus provides primary filtration for the urinary system, glomerular disease should be suspected when urine contains findings consistent with abnormal filtration: (4)
dysmorphic red cells, red cell casts, significant proteinuria, or lipiduria.
65
Nephritis, characterized by _________ (2), leads to ________ (2). The immunologic injury that characterizes glomerulonephritis can be subdivided into _________ (less than half of glomeruli affected) or _________ pathologies.
glomerular inflammation and/or necrosis
hematuria with proteinuria
focal nephritic; diffuse nephritic (Focal nephritic diseases tend to present with less severe proteinuria, while diffuse nephritis may lead to severe proteinuria such as that seen in nephrosis).
66
Nephritis and nephrosis each cause what type of glomerular injury?
inflammation (nephritis)
| alteration of the permeability of the glomerular membrane (nephrosis).
67
The most common glomerular diseases in adults include ________(5).
diabetic kidney disease, IgA nephropathy, rapidly progressive glomerulonephritis, minimal change disease, and membranous nephropathy.
68
The major clinical syndromes of glomerular disease are ________ and _________. Which can lead to chronic kidney disease?
acute glomerulonephritis (including rapidly progressive glomerulonephritis)
nephrotic syndrome
Either can lead to chronic kidney disease.
69
Glomerulonephritic pathologies (3)
- IgA nephropathy
- poststreptococcal glomerulonephritis
- rapidly progressive glomerulonephritis (RPGN)/crescentic glomerulonephritis - can be due to a number of conditions (see other card)
70
All of the following conditions may present with mild focal nephritis or more aggressive diffuse nephritis, including RPGN: (3)
What are the % of each?
1 Anti-GBM disease (20%)
2 Immune complex disease (40%)
3 Pauci-immune (ANCA) disease (40%)
71
Nephrosis commonly results from: (6)
- Diabetes mellitus
- Systemic lupus erythematosus (SLE)
- Amyloidosis
- Membranous nephropathy
- Minimal change disease
- Focal glomerulosclerosis
72
Nephrosis, characterized by abnormal permeability of the glomerular membrane, results in what in the urine? (2)
Are hematuria and cellular casts seen?
heavy proteinuria and lipiduria, since macromolecules such as albumin are allowed to pass.
The pathogenesis is less inflammatory than in nephritis; hematuria and cellular casts are generally not seen (but can be present). In classic forms, the nephrotic syndrome (see later) develops, but lesser degrees of proteinuria can be seen.
73
Membranous nephropathy - one of the most common causes of nephrotic syndrome in nondiabetics, characterized by _________. May be triggered by ________ (3). Nephrotic or nephritic?
diffuse thickening of the glomerular basement membrane due to in-situ immune complexes against a deposited antigen.
medications, underlying infections (hepatitis B), or malignancies (breast, colon, other solid tumors)
Nephrotic
74
Minimal change disease is characterized by __________ on immunofluorescence and ________ on EM. Nephrotic or nephritic?
lack of abnormality on light microscopy or IF, with electron microscopy showing flattening of glomerular epithelial cells.
Nephrotic - While minimal in detectable pathology, the resultant proteinuria can be massive, even rising above 8 to 9 g daily.
75
Focal glomerulosclerosis results in ________ (in the glomerulus), with microscopy showing ________ (2). Nephrotic or nephritic?
focal scarring involving only scattered glomeruli and segments of the glomerular tufts
immunoglobulin deposits and obliteration of the foot processes.
Nephrotic
76
Anti-GBM disease: mechanism? What is seen on IF microscopy? What disease is assoc with it? Nephrotic or nephritic?
Direct glomerular damage due to inflammation triggered by antibodies directed against components of the glomerular BM. Linear deposits of immunoglobulin are seen by immunofluorescence microscopy. The circulating antibodies may also lead to pulmonary hemorrhage, causing Goodpasture syndrome.
Nephritic.
77
Immune complex disease: mechanism? What is seen on IF microscopy? Classic lab finding? Nephrotic or nephritic?
Glomerular deposition of immune complexes (antibody-antigen) that result in an inflammatory response. IF reveals granular immunoglobulin deposits. Often associated with low serum complement levels.
Nephritic.
78
Pauci-immune disease: characterized by? Assoc with? What is seen on IF microscopy? Nephrotic or nephritic?
Group of disorders characterized by the presence of ANCAs, associated with multisystemic disease. Minimal or no immunoglobulin is seen by IF, hence the name “pauci-immune,” but glomerular injury is still believed to be immunologic. Considered to be part of the Wegener granulomatosis spectrum of diseases, and patients should be watched carefully for signs of systemic vasculitis.
Nephritic.
79
IgA nephropathy - relative incidence? Cause? Nephrotic or nephritic?
The most commonly found glomerulonephritic pathology (though rare in black individuals); caused by deposition of IgA with resultant inflammation and mesangial cell proliferation.
Nephritic.
80
Poststreptococcal glomerulonephritis: timing, glomerular findings? Tx? Nephrotic or nephritic?
Deposits of antigen are found humped in the subepithelial region; may develop 2 to 3 weeks after pharyngitis or cellulitis. Tx is usually supportive +/- antibiotics as necessary since it is usually a self-limiting condition.
Nephritic.
81
Rapidly progressive glomerulonephritis (RPGN)/crescentic glomerulonephritis - characterized by? Time course? Nephrotic or nephritic?
Extensive formation of extracapillary crescents in more than half of glomeruli; can be due to several conditions (see other card). RPGN refers to acute glomerulonephritis that advances to end-stage renal disease in days to weeks.
Nephritic.
82
Acute nephritis is characterized by the abrupt onset of _________ (5). These symptoms may be preceded by which Sx? (2)
hematuria, hypertension, edema, oliguria, and azotemia
| insidious and nonspecific symptoms of fatigue with edema
83
Nephrotic syndrome is defined as ____________. Resultant secondary findings include __________ (5). Other features (onset, gross hematuria, azotemia)?
proteinuria in excess of 3 g per day
hypoalbuminemia, edema, hyperlipidemia, and coagulation abnormalities (increased risk for DVT and renal vein thrombosis)
- The onset of nephrotic syndrome can be insidious.
- Gross hematuria is rare, and patients may present without azotemia.
84
Can any acute glomerular disease can lead to CKD?
| Advanced CKD can lead to ________ (6)
Yes
volume overload, hyperkalemia, metabolic acidosis, hypertension, anemia, and bone disease
(The onset of end-stage renal disease results in signs and symptoms of uremic syndrome)
85
Hemoptysis and renal disease DDx (4)
-most common: antiGBM (Goodpasture) disease
-ANCA-associated vasculitis with glomerulonephritis and pulmonary capillaritis (Wegener disease) - but upper respiratory tract involvement is more common.
(can be differentiated using serology +/- biopsy)
Less common causes of pulmonary-renal syndrome:
- SLE
- Henoch-Schonlein purpura.
86
Renal-dermal syndromes include: (4)
| What type of skin involvement is seen? (4)
SLE, Henoch-Schönlein purpura (HSP), cryoglobulinemia, and ANCA-associated vasculitis.
In these syndromes, dermal involvement may include palpable purpura (HSP), necrotic dermal inflammation, ulcers, or nodules.
87
Renal biopsy with examination by light microscopy, immunofluorescence, and electron microscopy is often useful for establishing a diagnosis in the setting of acute nephritis, RPGN, and nephrotic syndrome. It is usually reserved for patients who have _________ (2). Performed in consultation with a nephrologist, it is a relatively safe procedure.
negative serology and an unclear clinical diagnosis
88
Tx for nephrosis/nephrotic syndrome, control of proteinuria can be accomplished by _________ (2). Severe edema is treated with _________ (2).
nonspecific treatments such as ACE inhibitors and angiotensin II receptor blockers
moderate salt restriction (1 to 2 g per day) and the careful use of loop diuretics (taking care to avoid volume depletion and prerenal azotemia)
89
Tx of glomerular diseases with immunosuppressive agents (e.g., steroids, cyclophosphamide, mycophenolate mofetil): for which diseases:
- are they usually recommended? (3)
- can they limit disease? (3)
- may they be considered? (2)
- are they not useful? (2)
usually recommended: Goodpasture syndrome, Wegener granulomatosis, and polyarteritis.
Can limit disease in: idiopathic nephrotic syndrome, lupus nephritis, and idiopathic RPGN.
May be considered in: IgA nephropathy, amyloidosis when presentations are severe.
Not useful in: poststreptococcal glomerulonephritis, acute nephritis in the setting of infections such as endocarditis.
90
Approximately _______% of patients with minimal change disease maintain baseline renal function.
95%
91
Calcium and oxalate normally form a supersaturated solution in urine, but most people do not form kidney stones in part because of the kidney's natural inhibitors such as _________ (3).
When this supersaturated balance is disturbed, what are 2 mechanisms of calcium and oxalate precipitation?
citrate or kidney proteins (Tamm-Horsfall mucoprotein and nephrocalcin).
calcium and oxalate may precipitate on their own (homogeneous nucleation) or, more commonly, crystallize on another source such as urate crystals, epithelial cells, or urinary casts (heterogeneous nucleation).
92
Dietary factors (5) and medical conditions (5) that can increase risk for nephrolithiasis include:
DIET:
low fluid intake
grapefruit juice intake
high sodium intake, with increased sodium excretion accompanied by increased passive calcium excretion
high protein intake, with associated rise in acid and uric acid production
low dietary calcium intake, which reduces gut binding of dietary oxalate therefore increasing oxalate absorption.
MEDICAL conditions: hyperparathyroidism, obesity, gout, diabetes, and renal tubular acidosis.
93
Acute flank pain + gross hematuria DDx (5)
```
Nephrolithiasis
Renal malignancy
Pyelonephritis
Glomerulonephritis
Trauma
```
94
Acute flank pain DDx (6)
```
Nephrolithiasis
Aortic dissection
Lumbar disk disease
Renal infarct
Intestinal disease/ischemia
Ectopic pregnancy
```
95
How to distinguish nephrolithiasis and glomerulonephritis on urinalysis?
Urine sediment in nephrolithiasis will reveal nondysmorphic cells and the absence of red cell casts, in contrast to glomerulonephritis.
96
____________ is the confirmatory radiologic test of choice for nephrolithiasis.
Noncontrast helical computed tomography (CT) scan
97
Nephrolithiasis Tx for hospitalized pts (Tx req'd for all pts, and 4 choices for procedures)
IV fluids and adequate analgesia.
Stones that are smaller than 5 mm usually pass on their own.
Larger stones may require: Extracorporeal shock wave lithotripsy (ESWL), Retrograde ureteroscopy, percutaneous nephrolithotomy. Open lithotomy is reserved for the most difficult cases
98
After passing/removal,
Calcium stones: sodium restriction and thiazide diuretics, both of which decrease calcium excretion, are used for hypercalciuria. Thiazide diuretics decrease serum potassium and urinary citrate, so potassium citrate should be given to these patients as well. A calcium-restricted diet is not recommended because it will encourage continued calcium wasting (from bone). In hyperoxaluria, decreased dietary oxalate, calcium supplements to bind oxalate (not to be used by patients with concurrent hypercalciuria), or cholestyramine to bind fatty acids, bile salts, and oxalate is used.
Uric acid stones: alkalinization of the urine to pH >6 using potassium citrate, dietary restriction (avoid meats, fish), and allopurinol.
Following surgical removal of struvite stones, a course of antibiotics is targeted against the offending organism.
For cystine stones, aggressive fluid intake (more than 4 L per day), alkalinization, and sodium restriction. Penicillamine forms a soluble complex with cystine to prevent stones, but its toxic side effects limit its use to patients who fail routine therapy. (Cystinuria, a rare cause of kidney stones, may be screened for with the nitroprusside test.)
99
Hematuria (the presence of blood in the urine) is a very common disorder and can be classified as gross or microscopic depending on __________. Normal individuals excrete up to _________ red blood cells (RBCs) into the urine each day; more than this is considered to be abnormal hematuria.
whether or not blood is visible to the naked eye
| 2 million
100
Most nephrologists accept up to ________ RBCs per hpf as normal in a routine urinalysis.
2 to 3
101
RBCs originating from glomerular disease are often ____________, whereas nonglomerular disease is associated with __________ RBCs
dysmorphic; normomorphic
102
Hematuria is detected by ________ (2).
| Up to _____% of patients with hematuria have an underlying malignancy.
the presence of hemoglobin on a urine dipstick or by a finding >2 to 3 RBCs per hpf on examination of a spun urine sediment
10%
103
_________ (3) are at increased risk for urinary tract malignancy.
Men over age 50, smokers, people treated with cyclophosphamide, and those using high dose analgesics
104
_______ is the usual first-line imaging technique due to its sensitivity to detect tumor.
Referral for consideration of cystoscopy is indicated when _________.
Helical CT
| nonglomerular bleeding persists.
105
Causes of hematuria: kidney (8), ureters (2), bladder (7), prostate/male reproductive tract (3), urethra (4), systemic/other (4)
Kidney:
Infection (pyelonephritis, tuberculosis, parasites)*
Nephrolithiasis*
Malignancy (renal cell carcinoma)
Trauma
Glomerular disease (vasculitis, idiopathic)
Cysts (single and polycystic disease)
Allergic interstitial nephritis (drug induced)
Ischemia (embolism, thrombosis, papillary necrosis)
Ureters:
Nephrolithiasis
Tumor
Endometriosis
Bladder:
Infection (bacterial cystitis, parasites)
Calculus*
Interstitial cystitis
Tumor
Vascular malformations (hemangiomas, telangiectasias)
Endometriosis
Drugs (e.g., hemorrhagic cystitis from cyclophosphamide)
Prostate/Male Reproductive Tract:
Infection (prostatitis, epididymitis)
Benign prostatic hypertrophy (BPH)
Tumor
```
Urethra:
Urethritis (gonococcal, nongonococcal)
Stricture
Calculus
Trauma
```
```
Systemic Illnesses/Other:
Intense exercise*
Coagulopathy
Thrombocytopenia
Hemoglobinopathy
```
106
```
Hematuria + each of the following DDx
Flank pain (6)
Dysuria (5)
Urethral discharge (1)
Weight loss (1)
Fever (3)
Nocturia (3)
```
Flank pain (pyelonephritis, nephrolithiasis, neoplasms, ischemia, glomerulonephritis, hemorrhagic cyst)
Dysuria (cystitis, pyelonephritis, prostatitis, BPH, urethritis)
Urethral discharge (urethritis)
Weight loss (tumor)
Fever (pyelonephritis, neoplasms, tuberculosis)
Nocturia (cystitis, BPH, pyelonephritis)
107
Other historical findings are associated with specific causes of hematuria and should be sought: (6)
Recent streptococcal infection (poststreptococcal glomerulonephritis)
Gross painless hematuria (bladder cancer, glomerulonephritis)
Recent heavy exercise (exertional hematuria)
History of nephrolithiasis
Medication history (allergic interstitial nephritis, hemorrhagic cystitis)
Travel (parasitic infections)
108
Family history of hematuria suggests ________ (4)
polycystic kidney disease or three common causes of isolated glomerular hematuria:
IgA nephropathy (the most common cause of nephritis in adults)
Alport syndrome (a.k.a. hereditary nephritis)
Thin basement membrane disease (a.k.a. benign familial nephritis)
109
Hematuria + each of the following DDx:
Skin lesions (eg. ecchymoses, petechiae (2)
Costovertebral angle tenderness (3)
Abdominal mass (2)
```
Skin lesions (coagulopathy, vasculitis)
Costovertebral angle tenderness (pyelonephritis, tumor, glomerulonephritis)
Abdominal mass (polycystic kidneys, renal cell cancer)
```
