Chapter 3 Nephrology

Insider’s Guide to Nephrology for The USMLE Step 1

Nephrology can be a tricky subject for many medical students, especially because mastering renal physiology requires comfort with and even manipulation of several formulas. Luckily, the scope of nephrology-related questions on the USMLE tends to be rather limited. Focus heavily on the subjects listed in First Aid and then use the cases in this chapter to then test your understanding of the material. Be sure to understand detailed principles regarding nephron function and activation of the renin-angiotensin-aldosterone system. With regard to renal pathology, the most commonly tested subjects include renal failure, glomerulonephritis, urinary tract infections (UTIs), and renal stones.

Clinical renal disease

Case 3-1

A 78-year-old man comes to the emergency room because of inability to urinate for the past 2 days and is experiencing lower abdominal pain. He admits to urinary difficulties over the last few years, including difficulty initiating his stream, a weak stream, nocturia, and dribbling after voiding. He denies taking any tricyclic antidepressants, antipsychotics, antihistamines, or sympathomimetic agents. On physical examination his bladder seems palpably enlarged, and a digital rectal examination reveals an enlarged prostate. Microscopic urine examination shows no hematuria or crystalluria. Routine laboratory tests show significantly elevated blood urea nitrogen (BUN) and creatinine and a high-normal prostate-specific antigen (PSA) of 3.8. An abdominal ultrasound reveals a markedly distended bladder and enlargement of the renal pelves.

1 What is the probable cause of this patient’s problems?

This patient has acute urinary retention, most likely secondary to occlusion of the bladder neck by benign prostatic hyperplasia (BPH). BPH will generally result in a mild elevation of PSA, but typically not high enough to prompt evaluation for prostate cancer (which is traditionally undertaken for PSA levels >4). Although total PSA levels are elevated in both BPH and prostate cancer, free PSA levels will only be elevated with BPH. The elevated BUN and creatinine strongly suggest that this patient also has acute renal failure.

2 What are the three etiologic classifications of acute renal failure?

Renal failure is classified as prerenal, renal (intrinsic), or postrenal (obstructive). This man’s renal failure clearly has an obstructive etiology. Acute bladder distention caused by long-standing BPH has resulted in bilateral hydronephrosis (dilated renal pelves) and acute renal failure. Figure 3-1 shows severe hydronephrosis from long-standing obstruction, with marked dilatation of the renal pelvis and calyces and loss of cortical parenchyma.

Figure 3-1 Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and thinning of the renal parenchyma.

(From Kumar V, Abbas AK, Fausto N: Robbins and Cotran Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2005.)

3 How is glomerular filtration rate (GFR) calculated?

The GFR can be calculated using the following formula:

where

K_f = filtration coefficient, a constant

P_G = hydrostatic pressure in the glomerular capillaries

P_B = hydrostatic pressure in Bowman’s capsule

Π_G = oncotic pressure in the glomerular capillaries

Π_B = oncotic pressure in Bowman’s capsule, typically 0

4 Why is the absence of hematuria on urinalysis important in establishing the diagnosis?

Urinary calculi (stones) can cause urinary tract obstruction and are often associated with hematuria or microscopic crystals in the urine. Stones can uncommonly cause obstructive renal failure, but usually only if they are present in the ureters bilaterally. Tumors of the bladder or ureters (either primary urothelial tumors or tumors that invade or compress the urinary tract) can also cause lower tract obstruction with renal failure and hematuria.

Broadly speaking, obstructive renal failure is usually caused by obstruction at the level of the bladder neck or the ureters. Other causes of obstruction at the level of the bladder include neurogenic bladder and medication effects. Another classic (albeit uncommon) cause of ureteral obstruction is encasement of the ureters by retroperitoneal fibrosis.

5 Why was it important to ask this patient about tricyclic antidepressants, antipsychotics, antihistamines, and sympathomimetics?

These classes of drugs can all cause urinary retention secondary to cholinergic blockade, which inhibits contraction of the detrusor muscle.

Tricyclic antidepressants (e.g., amitriptyline, imipramine); the phenothiazine antipsychotics, which include low-potency “typical” antipsychotics such as chlorpromazine and thioridazine; and first-generation antihistamines such as diphenhydramine (Benadryl) are all older “dirty” agents that act on a multitude of receptor types, including muscarinic acetylcholine receptors. Hence, common side effects of these drugs include various anticholinergic actions such as dry mouth, constipation, and urinary retention. Recall that the detrusor muscle of the bladder is stimulated to contract by parasympathetic (cholinergic) innervation. The anticholinergic agent atropine has a similar effect. The anticholinergic effects of the widely used agents oxybutynin (Ditropan) and tolterodine (Detrol) are used therapeutically to control urge incontinence.

The sympathomimetics, on the other hand, can cause urinary retention by increasing the tone of the internal urethral sphincter.

Opiates (i.e., narcotics) have many anticholinergic-like side effects and (in addition to constipation, dry mouth, pupillary constriction, etc.) can cause acute urinary retention when given in high doses.

Summary Box: Obstructive Acute Renal Failure

The causes of acute renal failure (ARF) are divided into three groups: prerenal, renal (intrinsic), and postrenal (obstructive).

Common causes of postrenal failure include benign prostatic hyperplasia (BPH) or prostate cancer, bladder tumors, and urinary retention (due to neurogenic bladder or anticholinergic, opiate, or sympathomimetic drugs). Unless present bilaterally, renal stones rarely lead to obstructive kidney failure.

The diagnosis of obstructive renal failure is made, in part, by detection of hydronephrosis (pelvicalicectasis) on renal ultrasound.

Case 3-2

A 68-year-old man experienced a ruptured abdominal aortic aneurysm and was rushed to the hospital and into the operating room (OR). During surgery, the surgeons had to clamp the abdominal aorta at a level superior to the renal arteries for a little over an hour. Although the patient survived the operation, the next morning he was found to have a severe acute decline in his renal function with a BUN of 75 mg/dL and creatinine of 3.2 mg/dL. His calculated GFR was depressed to ~ 10 mL/min, his urine output diminished to ~ 200 mL in 24 hours (despite his being normotensive), and a urine microscopy revealed “muddy brown” granular casts.

1 What is the probable diagnosis?

The likely diagnosis is acute tubular necrosis (ATN), secondary to prolonged ischemia during the operation.

2 What is the pathophysiology of acute tubular necrosis?

In ATN, the renal tubular epithelial cells are damaged and sloughed off from the tubular basement membrane. These sloughed cells can be formed by the tubules into epithelial cell casts. Such casts can sometimes be seen in the urine of patients with ATN. More commonly, the epithelial cell casts have been degraded somewhat into pigmented “muddy brown” granular casts that, like the epithelial cell casts, are highly suggestive of ATN. In some cases, the urine sediment will reveal nonpigmented transparent hyaline granular casts; such casts can be formed from further degradation of “muddy brown” casts, but they can also be formed from other processes as well and so are not specific for ATN.

ATN can be ischemic or toxic. That is, the tubular epithelium can be damaged by either ischemia (as in this patient) or by nephrotoxins such as the chemotherapeutic agent cisplatin, aminoglycoside antibiotics, the antifungal amphotericin B, intravenous radiographic contrast media, heavy metals (Fanconi syndrome), and the heme pigments myoglobin and hemoglobin.

3 What is the cause of the decreased glomerular filtration rate and oliguria seen in acute tubular necrosis?

The sloughed tubular epithelial cells block the lumen of the renal tubules, impeding urine flow. Additionally, the denuded areas of basement membrane allow back-leakage of filtered fluid. Although this back-leakage does not change the amount of fluid filtered across the glomerular membrane, it does change the amount of waste products that are excreted, which consequently changes the calculated GFR.

Both the obstruction to flow and the back-leakage explain why overall urine output is frequently reduced in ATN.

4 What are the three phases of acute tubular necrosis?

In the initiation phase, the injurious agent or condition is present, but the deterioration of renal function has not yet begun or is just beginning. In the maintenance phase, GFR is reduced and oliguria persists; it is at this time that uremic complications are likely to manifest. Finally, in the recovery phase, renal tubular epithelial cells proliferate and repopulate the denuded areas, and urine output normalizes.

5 Other than the presence of “muddy brown” casts, how can prerenal azotemia due to ischemia be differentiated from ischemic acute tubular necrosis?

In clinical practice, this is a very important distinction to make, because prerenal azotemia (by definition) will respond to fluid resuscitation, whereas ischemic ATN will not.

In prerenal azotemia, inadequate renal perfusion reduces GFR, but the reduced perfusion is not so severe as to cause cellular damage. The kidneys therefore function normally in response to the hypoperfusion by retaining Na⁺. This typically results in a decreased fractional excretion (FE) of Na⁺ (FENa⁺) to below 1%. FENa⁺ is simply the ratio of urine sodium to plasma sodium, but with each value normalized according to (i.e., divided by) the corresponding creatinine concentration:

where

C_X = clearance of substance X; volume of plasma from which substance X is cleared per unit time

U_X = excretion rate of substance X

V = urine volume

P_X = plasma concentration of substance X

Cr = creatinine

If the hypoperfusion is severe enough, prerenal azotemia will progress, resulting in the ischemic damage to the tubular epithelium that is characteristic of ATN. In ATN, because many of the tubular cells are no longer functional, the kidney is unable to retain Na⁺ as it should in the setting of decreased GFR. As a result, the FENa⁺ in ATN is typically >2%.

In addition to the FENa⁺, the BUN/creatinine ratio can sometimes be useful in distinguishing between prerenal azotemia and ATN. Urea is primarily reabsorbed in the proximal tubule. In the setting of low extracellular volume (ECV), the increased Na⁺ reabsorption in the proximal tubule (as stimulated by angiotensin II, the sympathetic nervous system, and intrinsic glomerular processes) will tend to pull additional urea out of the filtrate through bulk flow. Thus, BUN can be used as a marker for proximal Na⁺ reabsorption. Creatinine, in contrast, is less affected by Na⁺ reabsorption (recall that creatinine is a useful marker for GFR because it is not significantly reabsorbed). Specifically in prerenal azotemia, one expects a BUN/Cr ratio elevated to >20. In ATN, in which the reabsorption of Na⁺ is impaired, this ratio is often <10 (damage to the renal tubules impairs urea reabsorption, so the BUN/Cr ratio is decreased). Although the BUN/Cr ratio is more readily available (as it requires only standard blood tests instead of both urine and blood), it is significantly less accurate than the FENa⁺ and can change independently of renal function. A classic example is a gastrointestinal (GI) bleed in which large amounts of the protein hemoglobin are broken down in the GI tract into urea that is extensively reabsorbed into the circulation, elevating the BUN level and the BUN/Cr ratio in a manner that is completely independent of renal function.

Related Question

6 What is rhabdomyolysis and how can it cause acute tubular necrosis?

Rhabdomyolysis is acute extensive destruction of skeletal muscle cells; it can occur with trauma (especially prolonged crush injuries), drugs (such as statins), and a host of other scenarios. With muscle injury, large amounts of the O₂ storage molecule myoglobin are released into the circulation and, upon arrival to the kidneys, lead to renal failure via multiple mechanisms. First, myoglobin is directly toxic to renal tubular epithelial cells. In addition, myoglobin can cause severe renal vasoconstriction (for poorly understood reasons), resulting in an ischemic component to the ATN. Finally, the released myoglobin can precipitate in the renal tubules and cause obstruction.

Contrast-induced ATN is similar to myoglobin-induced ATN in that it involves both direct toxic and vasoconstrictive/ischemic components, though the primary mechanism occurs through vasoconstriction. Contrast-induced ATN can be prevented with N-acetylcysteine, which is also used for cystic fibrosis treatment and acetaminophen toxicity.

Summary Box: Acute Tubular Necrosis

ATN is the most common cause of instrinsic renal failure.

ATN can be ischemic or toxic. Toxins capable of causing ATN include cisplatin, aminoglycosides, vancomycin, amphotericin, intravenous contrast agents, and myoglobin.

Ischemic ATN is distinguished from prerenal azotemia by the presence of “muddy brown” casts in the urinary sediment and an FENa⁺ >2%. Prerenal azotemia, in contrast, is characterized by a bland sediment, by a FENa⁺ <1%, and (less reliably) by a blood urea nitrogen/creatinine (BUN/Cr) ratio >20.

Case 3-3

A 53-year-old white female patient develops mediastinitis following coronary bypass surgery. She becomes septic with multiorgan failure, requiring intensive care unit (ICU) admission, intubation, pressor support, and hemodialysis. Her sternal wound is surgically débrided, and intraoperative cultures grow methicillin-sensitive Staphylococcus aureus. After 1 week, she is discharged home on long-term intravenous nafcillin. Ten days after discharge, she returns to the emergency department complaining of several days of fever, nausea, malaise, and rash. On examination, she is febrile to 38.7° C, and she has a full body, intensely erythematous maculopapular rash. Initial laboratory findings are most notable for an elevated creatinine of 3.9 mg/dL; her creatinine had completely normalized prior to discharge. Her white blood cell (WBC) count is also moderately elevated at 12 units, with a differential of 62% neutrophils, 22% lymphocytes, 12% eosinophils, and 4% monocytes.

1 What is the most likely cause for her acute renal failure?

This presentation is most consistent with acute interstitial nephritis (AIN) caused by nafcillin. AIN is most commonly an allergic reaction to a drug. Common culprits include antibiotics, particularly β-lactams (especially penicillins and cephalosporins) and sulfonamides; nonsteroidal anti-inflammatory drugs (NSAIDs); cimetidine; and proton pump inhibitors (PPIs), such as omeprazole and pantoprazole. AIN is less commonly caused by infections and is rarely a manifestation of an autoimmune disease (such as sarcoidosis).

In a setting of ARF, the triad of fever, rash, and peripheral eosinophilia following initiation of new medication is highly suggestive of AIN, but all three of these nonrenal manifestations are present in only a minority of patients. Urine microscopy may show WBCs, WBC casts, and red blood cells. Urine eosinophils are highly suggestive, but may not be present in all cases. When the diagnosis of AIN is unclear, biopsy can be performed, but often empiric therapy with corticosteroids is attempted first.

2 What are the three major types of NSAID-induced renal toxicity?

NSAIDs can cause a bewildering array of renal side effects.

In addition to interstitial nephritis, NSAIDs can also cause nephrotic syndrome. This typically manifests as minimal change disease in an adult taking NSAIDs, but other types of glomerular processes (such as membranous nephropathy) are possible as well.

The most common renal toxicity of NSAIDs is hemodynamically mediated acute renal failure. In the normal kidney, vasodilatory prostaglandins, such as PGI₂ (prostacyclin) and PGE₂, are produced to help maintain adequate renal perfusion. The enzyme cyclooxygenase (COX) is required for prostaglandin production. NSAID administration and the resultant inhibition of cyclooxygenase-1 or – 2 by NSAIDs can result in vasoconstriction of the renal arterioles, renal hypoperfusion, and a dramatic decrease in GFR. Risk factors for NSAID-induced renal failure include age >65 years, baseline renal dysfunction, and intravascular volume depletion (e.g., diuretic use and cirrhosis). This is in part because such patients with renal dysfunction or volume depletion depend more heavily than normal on prostaglandin production to maintain adequate renal perfusion.

Step 1 Secret

Nonsteroidal anti-inflammatory drug (NSAID)-induced decrease in glomerular filtration rate (GFR) is an important concept to know for Step 1. In general, you should be aware of all of the mechanisms by which GFR and filtration fraction can be altered. You are likely to be asked a question on this topic.

Step 1 Secret

Remembering the most common conditions that cause eosinophilia can be helpful. These conditions include helminthic infections, asthma and allergic disorders, drug-induced acute interstitial nephritis (AIN), and certain forms of malignancy (e.g., Hodgkin’s lymphoma).

Summary Box: Acute Interstitial Nephritis

Acute interstitial nephriyis (AIN) is classically characterized by the triad of fever, rash, and peripheral eosinophilia in a setting of ARF after introduction of a new drug. Urine eosinophils, although often not present, are also highly suggestive of AIN.

Agents associated with AIN include penicillins, cephalosporins, sulfonamides, nonsteroidal anti-inflammatory drugs (NSAIDs), and PPIs.

NSAIDs can cause AIN, nephrotic syndrome, and most commonly, hemodynamic renal failure from inhibition of vasodilatory prostaglandins. Patients with advanced age, renal dysfunction, or low effective circulating volume (e.g., congestive heart failure [CHF]) are at highest risk for NSAID-induced acute renal failure (ARF).

Case 3-4

A 65-year-old African-American woman with a long history of poorly controlled hypertension is evaluated for an elevated plasma creatinine that has been noted on routine laboratory tests over the past 6 months. Additional laboratory findings include hyperkalemia, hypocalcemia, hyperphosphatemia, and a metabolic acidosis. Hemoglobin A_1c and fasting glucose values are both normal. Urine microscopy does not reveal any hematuria or casts.

1 What is most likely causing her blood urea nitrogen and creatinine elevation?

She has renal failure resulting from a long history of poorly controlled hypertension. Hypertension is the second most common cause of chronic kidney disease. Renal failure from hypertension is particularly common in African Americans.

The pathologic changes associated with longstanding hypertension are termed hypertensive nephrosclerosis (also known as benign nephrosclerosis or hyaline arteriolar nephrosclerosis). As shown in Figure 3-2, hyaline arteriosclerosis is associated with hyaline deposition, marked thickening of the walls, and a narrowed lumen.

Figure 3-2 Hyaline arteriolosclerosis. High-power view of two arterioles with hyaline deposition, marked thickening of the walls, and a narrowed lumen.

(Courtesy of Dr. M.A. Venkatachalam, Department of Pathology, University of Texas Health Sciences Center, San Antonio, TX.)

2 What is the value of the normal fasting glucose and hemoglobin A_1c levels in the differential diagnosis?

This finding essentially rules out a component of diabetic nephropathy, the most common cause of chronic renal failure (CRF).

3 What is the difficulty in establishing that this patient’s renal failure was definitely due to hypertension, even if no other specific disease processes can be identified on renal biopsy?

The difficulty stems from the fact that hypertension is both a potential cause and a potential result of renal disease. Furthermore, if renal failure is chronic, renal biopsy findings can be nonspecific and may fail to distinguish between other precipitating insults. For example, her renal failure may have been due to a bout of glomerulonephritis that permanently damaged the kidneys, and her hypertension could have resulted from the kidney damage. Nevertheless, hypertension, regardless of its cause, contributes to progressive loss of renal function.

4 How does this woman’s renal failure explain her hypocalcemia?

In general, renal dysfunction leads to the accumulation of the various electrolytes that are normally excreted by the kidneys, resulting in hyperkalemia, hyperphosphatemia, and acidosis typical of renal failure. Calcium is rather unusual in that its serum levels may be decreased in renal failure. Keep in mind that in clinical practice, true hypocalcemia with chronic renal failure is rare due to the rapid compensatory increase in serum PTH levels that is mediated by the parathyroid glands.

When it does occur, hypocalcemia results from several processes. First, the kidney is the site of 1,25-dihydroxyvitamin D (i.e., calcitriol) synthesis from 25-hydroxyvitamin D, via the activity of renal α₁-hydroxylase in the proximal tubule. Since the 1,25-dihydroxy form of vitamin D is the active form that stimulates intestinal calcium absorption, loss of renal parenchyma reduces synthesis of this compound and reduces intestinal calcium absorption. Second, as GFR declines, renal phosphate excretion declines and leads to hyperphosphatemia. This elevated serum phosphate can complex with serum calcium and reduce free ionized calcium levels. In addition, the increased phosphate, through negative feedback, also inhibits the synthesis of 1,25-dihydroxyvitamin D. (Recall that 1,25-dihydroxyvitamin D tends to increase serum levels of both Ca²⁺ and phosphate as it promotes the intestinal absorption of both substances. Parathyroid hormone [PTH], on the other hand, increases serum calcium levels while promoting phosphate excretion at the level of the kidney.)

Note: There are two forms of vitamin D: plant-derived vitamin D₂ (ergocalciferol) is acquired in our diets; vitamin D₃ is made endogenously in our skin in a reaction that is catalyzed by ultraviolet (UV) rays (i.e., sunlight). In order to become biologically active, both vitamin D₂ and D₃ must be hydroxylated twice. The first hydroxylation is unregulated and occurs in the liver to produce the 25-hydroxyvitamin D diol form. The second step, which is impaired in renal failure, is highly regulated and produces the 1,25-dihydroxyvitamin D triol form (hence the name calcitriol).

5 Would parathyroid hormone levels be increased or decreased in this patient?

Because PTH is released in response to hypocalcemia (or hyperphosphatemia), PTH levels are increased in renal failure.

Because this increase in PTH is reactive in nature (i.e., an appropriate response to the hypocalcemia and hyperphosphatemia of renal failure), it is termed secondary hyperparathyroidism. Patients in early renal failure will often have a high PTH level with relatively normal serum calcium. However, in severe renal failure, as both 1,25-hydroxyvitamin D levels decrease and phosphate levels increase to a greater extent, the progressively elevated PTH levels are unable to compensate, and progressively severe hypocalcemia develops.

Note: Primary hyperparathyroidism, in which an abnormality of the parathyroid gland (typically glandular hyperplasia or an adenoma) results in increased PTH levels as a primary disturbance, causes hypercalcemia rather than hypocalcemia.

6 How does parathyroid hormone normally act to regulate serum Ca²⁺? How are parathyroid hormone levels normally regulated?

The various actions of PTH act overall to increase serum Ca²⁺ while maintaining serum phosphate levels.

First of all, PTH stimulates bone reabsorption, which releases Ca²⁺ and phosphate into circulation. It also stimulates activation of vitamin D by stimulating the activity of α₁-hydroxylase in the proximal tubule. The active 1,25-dihydroxyvitamin D then increases intestinal absorption of Ca²⁺ and phosphate and (at high levels) promotes bone resorption, again acting to increase serum levels of both Ca²⁺ and phosphate. Finally, PTH stimulates Ca²⁺ reabsorption at the level of the kidney while strongly promoting phosphate excretion.

Thus, PTH acts directly and indirectly at bone, the GI tract, and the kidneys to increase plasma Ca²⁺. However, because the phosphate released from bone and absorbed from the GI tract is excreted in the kidneys, the combination of PTH and vitamin D activation tends to have no net effect on serum phosphate.

In general, PTH release is stimulated by low Ca²⁺ levels, whereas its release is inhibited (in a negative feedback mechanism) by the active 1,25-dihydroxy form of vitamin D (Fig. 3-3).

Figure 3-3 Parathyroid hormone (PTH) overview.

(From Brown TA: Rapid Review Physiology. Philadelphia, Mosby, 2007, p 128.)

7 What are the potential pathologic manifestations of the hyperparathyroidism that develops in renal failure?

Although the elevated PTH seen in renal failure is an appropriate response to hypocalcemia, it has a negative impact on bone metabolism. The chronically high PTH levels stimulate chronic bone resorption, which can result in osteoporosis as well as abnormal cysts in areas of demineralized bone (osteitis fibrosa cystica).

In the chronic management of renal failure, in addition to the maintenance of relatively normal calcium and phosphate concentrations, a relatively normal PTH level is also an important therapeutic goal that often requires specific drug therapy. The agents used include active vitamin D analogs (that have negative feedback on PTH release) as well as newer agents that suppress PTH release by mimicking the action of calcium on the parathyroid gland.

Step 1 Secret

Parathyroid hormone (PTH) and vitamin D are routinely tested topics on the USMLE. It is very important to understand the difference between primary and secondary hyperparathyroidism and to know which conditions elevate levels of PTH and vitamin D.

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Apr 7, 2017 | Posted by admin in NURSING | Comments Off

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Nephrology

Clinical renal disease

Case 3-1

1 What is the probable cause of this patient’s problems?

2 What are the three etiologic classifications of acute renal failure?

3 How is glomerular filtration rate (GFR) calculated?

4 Why is the absence of hematuria on urinalysis important in establishing the diagnosis?

5 Why was it important to ask this patient about tricyclic antidepressants, antipsychotics, antihistamines, and sympathomimetics?

Case 3-2

1 What is the probable diagnosis?

2 What is the pathophysiology of acute tubular necrosis?

3 What is the cause of the decreased glomerular filtration rate and oliguria seen in acute tubular necrosis?

4 What are the three phases of acute tubular necrosis?

5 Other than the presence of “muddy brown” casts, how can prerenal azotemia due to ischemia be differentiated from ischemic acute tubular necrosis?

Related Question

6 What is rhabdomyolysis and how can it cause acute tubular necrosis?

Case 3-3

1 What is the most likely cause for her acute renal failure?

2 What are the three major types of NSAID-induced renal toxicity?

Case 3-4

1 What is most likely causing her blood urea nitrogen and creatinine elevation?

2 What is the value of the normal fasting glucose and hemoglobin A_1c levels in the differential diagnosis?

3 What is the difficulty in establishing that this patient’s renal failure was definitely due to hypertension, even if no other specific disease processes can be identified on renal biopsy?

4 How does this woman’s renal failure explain her hypocalcemia?

5 Would parathyroid hormone levels be increased or decreased in this patient?

6 How does parathyroid hormone normally act to regulate serum Ca²⁺? How are parathyroid hormone levels normally regulated?

7 What are the potential pathologic manifestations of the hyperparathyroidism that develops in renal failure?

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