Renal Flashcards
What is the most likely diagnosis?
The patient most likely has acute tubular necrosis (ATN) secondary to renal ischemia as a consequence of shock due to the accident. ATN is the most common cause of acute kidney injury and is a result of direct injury to the renal tubular epithelia.
What are common causes of Acute Tubular Necrosis?
Renal ischemia and nephrotoxins are the two general classes of causes of ATN. Hypotension and other prerenal diseases can cause renal ischemia. Common nephrotoxins include antibiotics (eg, aminoglycosides, amphotericin, foscarnet), radiocontrast, immunosuppressants (eg, cyclosporine, tacrolimus), chemotherapy agents (eg, cisplatin), and myoglobin (eg, in rhabdomyolysis).
What is the cause of the patient’s azotemia in Acute Tubular Necrosis?
ATN involves direct damage to renal tubular epithelial cells (the proximal tubule is particularly vulnerable to ischemic injury because of its high demand for adenosine triphosphate). In addition, the sloughing of intact tubular cells and necrotic cellular debris into the tubular lumen blocks the urinary luminal tract. This leads to a back leak of the filtrate and, consequently, a decrease in the glomerular filtration rate (GFR).
How do the laboratory findings help distinguish Acute Tubular Necrosis from prerenal disease?
Why is the BUN/creatinine ratio elevated in prerenal disease but not in intrinsic renal disease?
most sensitive to hypoperfusion) where volume depletion increases reabsorption of sodium and water in parallel with an increase in BUN.
Creatinine is not reabsorbed in the proximal tubule; hence, when there is volume depletion, there is not a commensurate rise in serum creatinine. Creatinine is freely filtered, and then gets secreted in the tubules.
Thus, in cases of upper gastrointestinal bleeding or other causes of hypoperfusion, BUN is elevated but creatinine is normal.
What is the natural course of Acute Tubular Necrosis?
Within 36 hours of injury, ATN undergoes an initiatory phase, during which time urine output decreases and BUN increases. Within 2–6 days, a maintenance phase begins, where urine output falls dramatically and there is a significant risk of death without treatment. Finally, the recovery phase typically occurs within 2–3 weeks.
How do the results of a fluid challenge test differ between Acute Tubular Necrosis and prerenal disease?
A fluid challenge (the use of intravenous fluids to restore intravascular fluids) usually restores normal renal function in patients with simple prerenal disease (hypoperfused kidneys). However, in patients with ATN, renal dysfunction often persists despite fluid challenge. A fluid challenge is contraindicated in patients with volume overload (eg, heart failure).
How do the urinary sodium excretion and FeNa values differ between Acute Tubular Necrosis and prerenal disease?
What is the most likely diagnosis?
Autosomal dominant polycystic kidney disease (ADPKD). ADPKD has a prevalence of approximately 1:1,000 and is the leading genetic cause of chronic renal failure. It is diagnosed with imaging.
How is Autosomal dominant polycystic kidney disease (ADPKD) inherited?
The disease is inherited in an autosomal dominant fashion. Approximately 85% of cases of ADPKD are due to a mutation in the PKD1 gene on chromosome 16; the remainder of the cases are caused by mutations in PKD2 on chromosome 4.
What is the presentation of Autosomal dominant polycystic kidney disease (ADPKD)?
ADPKD may present at any age but is most frequently diagnosed in the third to fifth decades (although PKD type 2 inheritance has a later onset). Because ADPKD is dominantly inherited, patients may be aware of a family history of the disease. Patients can experience chronic flank pain due to calculi, urinary tract infection, or massively enlarged kidneys. Patients may also present with gross hematuria, and nocturia may be present if renal concentrating ability is impaired. Upon presentation, microscopic hematuria and proteinuria may be found, and hypertension at presentation is common.
What are the extrarenal manifestations of Autosomal dominant polycystic kidney disease (ADPKD)?
Colonic diverticular disease is the most common extrarenal effect of ADPKD. Hepatic cysts (Figure 12-1) are present in 50%–70% of patients and are generally asymptomatic with little effect on liver function. There is also an association between ADPKD and berry aneurysms of the circle of Willis, which show familial clustering. Rupture of such aneurysms results in subarachnoid hemorrhage and increased mortality and morbidity. Mitral valve prolapse is found in 25% of patients with this disease. Most patients with APDKD die from cardiac causes. Cardiac hypertrophy and coronary disease are extremely common.
What is the prognosis for patients with Autosomal dominant polycystic kidney disease (ADPKD)?
Progression to chronic renal failure is common, with 50% of patients developing end-stage renal disease by 60 years of age (ADPKD accounts for approximately 5% of patients who initiate dialysis annually). There is great variability in the progression of the disease even within families. Early age at diagnosis, male gender, recurrent infection, proteinuria, and hypertension are all associated with an early onset of renal failure. PKD1 carriers tend to have a more severe course. At present, there is no proven treatment for ADPKD; management generally consists of controlling any associated hypertension and/or proteinuria to preserve the glomerular filtration rate, but renal replacement therapy is eventually indicated.
What is the most likely diagnosis?
The most common causes of gross hematuria in a child are urinary tract infection and trauma. The most likely diagnosis in this case, however, is hereditary nephritis, or Alport syndrome, which consists of glomerular disease, sensorineural deafness, and ocular abnormalities, such as anterior lenticonus, a conical projection of the lens surface. These patients often progress to end-stage renal disease by the second decade of life.
Alport syndrome is due to a mutation in a gene that codes for which protein?
Because of this mutation, the glomerulus loses the ability to selectively filter on the basis of what property?
Alport syndrome is due to a defect in the gene that codes for the α5 subunit of type IV collagen. Type IV collagen is found primarily in the basal lamina. Tissue from patients with this mutation fails to stain for this protein.
The glomerulus loses the ability to filter on the basis of size. The glomerular basement membrane is primarily a size-selective (as well as charge-selective) filter; therefore, damage to the basement membrane leads to loss of size selectivity.
What is the probability that this patient’s brother (person 3 in Figure 12-2) also has Alport Syndrome?
The probability is 50%. The pedigree represents X-linked inheritance. Since the boy’s mother is a carrier, each son has a 50% chance (one of two X chromosomes in the mother) of inheriting the mutation. There are also autosomal recessive and autosomal dominant variants of Alport syndrome.
What other screening tests, in addition to urinalysis, can be used to confirm the diagnosis of Alport syndrome?
Alport syndrome is associated with ocular abnormalities and deafness; therefore, an ophthalmological examination and a formal audiogram should be performed, as deficits may be subtle. Skin biopsies can also be useful in diagnosing Alport syndrome.
What is the most likely diagnosis?
There is a high clinical suspicion for drug-induced acute interstitial nephritis (AIN) because of the patient’s recent initiation of a medication. Drug therapy is responsible for 71% of reported AIN cases, with infections (eg, Legionella, leptospirosis, cytomegalovirus, and streptococci) and autoimmune disorders (eg, systemic lupus erythematosus, Sjögren syndrome, sarcoidosis) responsible for the rest. AIN can develop between 1 week and 9 months of drug initiation.
What drugs are associated with drug-induced acute interstitial nephritis (AIN)?
Many medications have been associated with AIN, although methicillin remains the classic drug.
What other symptoms are common in patients with drug-induced acute interstitial nephritis (AIN)?
Other nonspecific complaints, such as weakness, fatigue, and anorexia, are common. Rash can sometimes accompany fever and eosinophilia to complete the classic triad of a drug-induced hypersensitivity reaction. However, only 10% of cases of drug-induced AIN manifest with all three signs.
What are the typical urinalysis findings in drug-induced acute interstitial nephritis (AIN)?
Urinalysis often reveals pyuria and hematuria. WBC casts in the absence of a urinary infection is highly suggestive of AIN. Urine eosinophils increase the suspicion as well. Mild proteinuria may be found. Creatinine concentration can also be acutely elevated.
What kidney biopsy findings are common in drug-induced acute interstitial nephritis (AIN)?
Kidney biopsy is the only way to confirm this condition. Renal tissue histopathology often shows interstitial edema with diffuse cellular infiltration of the interstitium by inflammatory cells including lymphocytes, monocytes, eosinophils, and granulocytes (Figure 12-3). Tubulitis may also be seen. The presence of granulomas may suggest an autoimmune cause, such as sarcoidosis.
What is the appropriate treatment for drug-induced acute interstitial nephritis (AIN)?
Withdrawal of the offending agent is the primary therapy. The effectiveness of corticosteroid treatment has not been proven by a prospective, randomized controlled trial, but prednisone is often used empirically, especially in cases of failure to induce remission after withdrawal of drug therapy or advanced renal failure.
What is the most likely diagnosis?
This patient has likely developed Fanconi syndrome (FS), which is characterized by a generalized transport defect in the proximal tubules, thus representing a proximal (type II) renal tubular acidosis (RTA). FS is either acquired or inherited. It can be acquired as a rare complication of plasma cell dyscrasias, including multiple myeloma, MGUS, Waldenström macroglobulinemia, and primary amyloidosis. FS may also result from Sjögren syndrome, heavy metal poisoning, and drug reactions. If inherited, FS is mostly transmitted as an autosomal recessive trait.
Although all of the urinalysis and laboratory findings support the diagnosis of FS, in a patient with MGUS and back pain, multiple myeloma should be on the differential.
What are the functions of the proximal convoluted tubules?
The proximal convoluted tubules are the “workhorses of the nephron” and reabsorb all glucose and amino acids and the majority of filtered sodium, potassium, phosphate, bicarbonate, and water. Ammonia is also secreted to buffer distally secreted H+.
What is the pathogenesis of Fanconi syndrome?
FS is characterized by multiple proximal tubular transport defects. The exact mechanism varies with the etiology of FS. In FS associated with monoclonal gammopathies, kappa-type Bence Jones proteins have been found to be reabsorbed by proximal tubular cells. Subsequent failure to complete proteolysis of these light chains results in cytoplasmic crystalline inclusions, which may eventually compromise tubular function.
What medication can mimic the presentation of Fanconi syndrome?
Acetazolamide works by inhibiting bicarbonate in the proximal tubule and thus can cause proximal RTA.
What is glomerular filtration rate (GFR)?
What is the mechanism of the observed hypokalemia in Fanconi syndrome?
The primary function of the kidneys is to preserve volume though the reabsorption of sodium and free water. In FS, there is an increased distal delivery of sodium due to the incompetent proximal tubules. The principal cells within the collecting ducts will compensate by increasing sodium reabsorption through an exchange for potassium. This results in potassium clearance rates that may be more than twice the GFR, indicating net tubular secretion. Metabolic acidosis secondary to defective proximal tubule bicarbonate reabsorption may also contribute to potassium loss, as cells tend to remove H+ from circulation through an exchange for potassium, thereby increasing the filtered load of potassium.
What conditions should be considered in the differential diagnosis?
Acute glomerulonephritis and alveolar hemorrhage suggest Goodpasture syndrome (GP) or a systemic vasculitis, such as Wegener granulomatosis or microscopic polyangiitis. While vasculitis is more common, that would likely present with constitutional symptoms. Lupus and other forms of acute glomerulonephritis that are related to pulmonary infection or result in pulmonary edema should also be considered.
To aid in the diagnosis, which 4 antibodies should be tested for by serology?
- Anti–glomerular basement membrane (anti-GBM) antibody
- Anti–neutrophilic cytoplasmic antibody (vasculitides)
- Anti-Smith antibody
- Anti–double-stranded DNA (lupus)
Only anti-GBM antibodies are subsequently isolated from the patient’s serum. What is the epidemiology of the associated condition?
Isolation of anti-GBM antibodies suggests Goodpasture syndrome, which is a form of anti-GBM disease characterized by rapidly progressive glomerulonephritis, alveolar hemorrhage, and autoantibodies to type IV collagen. GP has a prevalence of 1:1 million. GP occurs with alveolar hemorrhage in 60%–70% of cases. Males 5–40 years of age are most commonly affected. Both genders are affected equally in older adults. Patients younger than 30 years of age are more likely to be severely affected. Untreated, GP has a fatality rate of 50%.
What is the pathogenesis of Goodpasture syndrome?
IgG (rarely IgA or IgM) autoantibodies against type IV collagen are the distinguishing feature of GP, and they also correlate with the severity of disease. The α3 chains of type IV collagen are present in the basement membranes of glomeruli, alveoli, and several other organs. The antigen targets of GP autoantibodies are normally inaccessible because of the presence of endothelial cells. The exposure of these antigens to circulating antibodies is more likely in the kidneys and lungs because of the fenestrated nature of the endothelial lining of glomerular capillaries and the increased susceptibility of the lungs to injury (eg, from smoking, toxin inhalation, or infection).
What type of hypersensitivity reaction is responsible for this patient’s disease process in Goodpasture syndrome?
A type II hypersensitivity reaction is responsible. Fixation of complement to the anti-GBM antibodies activates the classic complement pathway that results in the recruitment of neutrophils and monocytes. Type II hypersensitivity is also seen in myasthenia gravis, pernicious anemia, Graves disease, pemphigus vulgaris, and other conditions.
What are the typical kidney biopsy microscopy findings in Goodpasture Syndrome?
Light microscopy typically shows cres- centic glomerulonephritis (see Figure 12-8). Immunofluorescence microscopy (Figure 12-4) demonstrates the nearly pathognomonic finding of a smooth linear deposition of IgG along the glo- merular capillaries.
What is the most likely diagnosis?
Henoch-Schönlein purpura (HSP). In children, the combination of rash (as described above), arthralgias, abdominal pain, and renal disease is pathognomonic for HSP. However, only 63% of patients with HSP actually present with abdominal pain and only 40% with renal disease. An additional 33% of patients also have evidence of gastrointestinal bleeding. Less common symptoms include testicular torsion, intussusception, pancreatitis, cholecystitis, and protein-losing enteropathy. Approximately 1% of children with HSP progress to end-stage renal disease, and approximately 10% of HSP cases are seen in adults.
What are the dermatologic findings for Henoch-Schönlein purpura (HSP)?
Both purpura and petechiae may be seen in HSP. Purpura is characterized by nonblanching, flat lesions measuring > 2 mm in diameter. Petechiae are non-blanching, flat lesions measuring < 2 mm in diameter. Both are signs of bleeding occurring in the skin.
What is the pathophysiology of Henoch-Schönlein purpura (HSP)?
HSP is a small-vessel vasculitis. Although the precipitating factor is unknown, anecdotal evidence suggests upper respiratory infection for children. With HSP, IgA deposition in blood vessels causes leaking, which leads to purpura and petechiae. This is pathophysiologically similar to IgA nephropathy.
Which conditions should be considered in the differential diagnosis of this patient’s rash?
The main concerns, in addition to HSP, are clotting disorders and sepsis; as a result, coagulation studies should be performed. A similar rash can be caused by rickettsial infections, although this patient is afebrile. It is important to distinguish HSP from hemolytic-uremic syndrome (HUS), as the two conditions present similarly and can both cause extensive renal disease. However, HUS is not likely in this patient, as there are no signs of hemolytic anemia such as schistocytes on blood smear. In adults, HSP must be distinguished from systemic diseases such as hypersensitivity vasculitis and systemic lupus erythematosus.
What are the appropriate treatments for Henoch-Schönlein purpura (HSP)?
Treatment is based on the severity of symptoms, as the disease is typically self-limiting. An asymptomatic patient requires no treatment. However, severe symptoms, including signs of renal involvement, may require renal biopsy and steroids. Regardless of the severity of symptoms, patients with HSP require urinalysis every 3 months for 1 year, as HSP has a high rate of recurrence. Recurrence or flares typically occur within 4 months of the initial diagnosis.
What is the most likely diagnosis?
Hypercalcemia. Symptoms include lethargy, hyporeflexia, confusion, depression, headaches, psychosis, bradycardia, a shortened QT interval, nausea, vomiting, constipation, muscle weakness, polyuria, polydipsia, and gastroduodenal ulcer disease (secondary to calcium-induced gastrin release).
How are ionized calcium and albumin used in the diagnosis of Hypercalcaemia?
Ionized calcium is the primary determinant of cellular and membrane activity. However, routine reporting of serum calcium levels includes calcium that is bound to proteins. Approximately 45% of calcium circulates in the free or ionized form, and another 40% is bound to albumin (the remainder is bound to various anions). Accurate assessment of calcium levels therefore requires the simultaneous measurement of albumin and serum calcium levels.
How does hypoalbuminemia affect Hypercalcaemia?
Hypoalbuminemia can decrease measured serum calcium levels independently of any net change in ionized calcium levels. For each decrease of 1.0 g/dL in serum albumin below the laboratory’s reference normal value, 0.8 mg/dL should be added to the total calcium measured (the opposite is done in cases of hyperalbuminemia). Given the patient’s hypoalbuminemia, the actual total serum calcium level is even greater than the already elevated total calcium observed.
What are the two most common causes of hypercalcemia?
Hyperparathyroidism (thus the importance of checking PTH levels) and malignancy are the leading causes of hypercalcemia.
What are the appropriate treatments for Hypercalcaemia?
Symptomatic hypercalcemia, as seen in this patient, should first be treated with a saline infusion to expedite renal calcium excretion. Furosemide may be initiated to promote calciuresis only after the patient is volume replete. Furosemide promotes natriuresis and increases calcium excretion. Bisphosphonates inhibit osteoclast activity and are also used to treat hypercalcemia. Given this patient’s history of chronic osteomyelitis, suppressed PTH, and dramatically elevated alkaline phosphatase levels, there is a high clinical suspicion for underlying malignancy.
What is the most likely diagnosis?
Hypokalemia
What two main factors predisposed the patient to torsades de pointes?
The patient was started on digoxin to increase cardiac output and to treat the atrial fibrillation; furosemide was added to treat the pulmonary edema. However, furosemide in the setting of congestive heart failure can lead to severe hypokalemia (serum potassium level < 2.5 mEq/L). Hypokalemia has been shown to promote digitalis-induced arrhythmias, even when digitalis levels are in the therapeutic range. Digitalis toxicity can induce fatal arrhythmias.
What are the most common causes of Hypokalaemia?
What is the most likely diagnosis?
Hyponatremia, which is commonly defined as a serum sodium concentration ≤ 135 mEq/L. Hyponatremia is more prevalent in the hospital setting or in nursing homes.
What are the common causes of Hyponatraemia?
What is the pathogenesis of this condition in this particular patient?
This patient is likely suffering from diuretic-induced hyponatremia. Thiazides deplete serum sodium and potassium levels and stimulate ADH-mediated water retention. It should be noted, though, that loop diuretics are unlikely to cause hyponatremia, as the maximal urine concentrating ability, and thereby water retention, is reduced with the decrease in medullary interstitial tonicity. If hyponatremia develops over a period of days rather than acutely, the brain cells react to hyponatremia by secreting salts and, over time, organic osmolyte to prevent excess water entry and swelling. This may explain why no significant swelling can be seen on CT scan of the head.
What is the most likely diagnosis?
Hypophosphatemic (previously vitamin D–resistant) rickets is suggested by the patient’s slow growth and skeletal findings as well as by his laboratory values: upper normal PTH, normal calcidiol and calcium levels with low calcitriol (which would normally be elevated in the setting of hypophosphatemia), and phosphaturia in the setting of normal renal function. Two inheritable forms exist. X-linked hypophosphatemic (XLH) rickets is more likely in this case, as it generally affects males and presents in childhood. The grandfather likely was similarly affected, whereas the heterozygous mother is only mildly affected with dentition problems. Less common autosomal dominant and recessive forms also exist, which affect both genders equally and present later in life.
What are the typical radiologic findings in Hypophosphatemic rickets?
Figure 12-5 shows the widened diaphyses, funnel-like beaking of the metaphyses, and increased curvature of the femoral and tibial shafts. Enthesopathy (calci- fication of tendons, ligaments, and joint capsules) is also often seen. Lower-extremity deformities develop as the child begins to bear weight with ambulation.
What is the acid-base disturbance in this patient?
What are the causes and two main types of metabolic acidosis?
How is anion gap calculated?
What is the pathogenesis of this patient’s condition?
Aspirin is hydrolyzed to salicylate once ingested. At toxic levels, salicylates cause a primary respiratory alkalosis by stimulating the medullary respiratory center to hyperventilate. Salicylates also stimulate skeletal muscle metabolism, increasing oxygen consumption and carbon dioxide production. This further stimulates hyperventilation. The metabolic acidosis component occurs because salicylates cause both lipolysis and uncoupling of oxidative phosphorylation, resulting in the production of organic acids, pyruvate, and ketones.
What acid-base disturbance is seen in this patient?
Metabolic alkalosis. The pH of the arterial blood is > 7.45, which indicates alkalemia. Metabolic alkalosis can be distinguished from respiratory alkalosis by examining the PCO2. Normal or increased PCO2 with increased bicarbonate indicates that the alkalosis is metabolic.
What does the body do to partially compensate for Metabolic alkalosis?
How is Metabolic alkalosis further classified?
What is the pathogenesis of this patient’s condition?
This patient is volume depleted because he stopped his intravenous fluids. In addition, he has been vomiting, which removes further fluid and chloride (from HCl). His alkalemia is therefore likely saline responsive. His dehydration stimulates the renin-angiotensin-aldosterone system. Elevated aldosterone causes reabsorption of Na+ in exchange for K+ and H+. This further exacerbates the alkalemia and also leads to hypokalemia. Treatment involves restoration of volume status to prevent further exacerbation of the alkalemia and the complications of hypokalemia.
What is the most likely diagnosis?
The boy likely has nephrotic syndrome in the form of minimal change disease (lipoid nephrosis). This is the most common manifestation of nephrotic syndrome in children (approximately 90% of cases occur in children younger than 10 years of age). Age younger than 6 years, normal renal function, and absence of hypertension are strong indicators for this diagnosis.
What are the four classic symptoms of Nephrotic syndrome?
Nephrotic syndrome classically presents with proteinuria, hypoalbuminemia, edema, and hypercholesterolemia (Table 12-1).
What are the likely histology findings in Nephrotic syndrome - minimal change disease?
Glomeruli appear normal on light microscopy, leading to the name minimal change. However, when the glomeruli are viewed under electron microscopy, effacement or flattening of foot processes can be seen. The electron micro- graph in Figure 12-6 shows ef- facement of the foot processes (arrowhead).
What is the most likely diagnosis? What is the most likely cause of this patient’s proteinuria?
The boy’s presentation suggests nephrotic syndrome, which is characterized by the triad of high urine protein losses, hypoalbuminemia, and hypercholesterolemia. Patients often present with periorbital edema, peripheral edema, and/or ascites secondary to decreased plasma protein. This results in decreased plasma oncotic pressure, which, in turn, leads to sodium and free water retention.
The likely mechanism of action is loss of charge barrier at the glomerular membrane due to effacement of foot processes (which would be seen on electron microscopy; no changes would be seen on light microscopy).
After 2 months of steroid treatment, the patient shows no decrease in his proteinuria, and a renal biopsy is obtained. What is the most likely diagnosis?
The boy likely has developed focal segmental glomerular sclerosis (Figure 12-7), which can be resistant to steroid treatment. Light microscopy of the biopsy specimen may demonstrate focal areas of glomeruli with segmental sclerosis. Electron microscopy demonstrates foot process derangement.
What is the most likely diagnosis?
The presence of flank pain, emesis, high fever, and costovertebral angle tenderness indicate acute pyelonephritis. Pyelonephritis is a urinary tract infection (UTI) that has progressed from the lower urinary tract (bladder/urethra) to the upper urinary tract. It is most common in young children and sexually active women. Men are less likely to develop pyelonephritis or acute cystitis, in part because of their longer, less exposed urethras. Other predisposing factors include vesicoureteric reflux (congenital), flow obstruction, catheterization, gynecologic abnormalities, diabetes, and pregnancy.
How can this patient’s symptoms be distinguished from those associated with cystitis, urethritis, or vaginitis?
Pyelonephritis classically manifests as flank pain, costovertebral angle tenderness, nausea, and vomiting with high fever. By contrast, the classic primary complaint in cystitis is dysuria accompanied by frequency, urgency, suprapubic pain, and hematuria. Urethritis and vaginitis present with dysuria, discharge, pruritus, dyspareunia, and an absence of frequency or urgency.
What classification of renal disorders do these symptoms represent?
Hematuria with RBC casts, dysmorphic RBCs, and proteinuria on urinalysis in the setting of hypertension and edema indicate a nephritic syndrome. Causes of nephritic syndrome include rapidly progressive glomerulonephritis (RPGN), poststreptococcal GN, IgA nephropathy, lupus nephritis, and mesangial proliferative GN.
The next day, the patient is oligo-anuric, and her serum creatinine rises to 3.2 mg/dL. What is the most likely diagnosis?
This patient most likely has RPGN, a clinical diagnosis characterized by a doubling of serum creatinine in a 3-month period and rapid progression to acute renal failure. RPGN can result from a primary glomerulopathy or a secondary glomerulopathy mediated by a systemic disease, such as lupus in this case, or a streptococcal infection.
Kidney biopsy is also performed the next day (Figure 12-8). How does it aid in the diagnosis of rapidly progressive glomerulonephritis (RPGN)?
Kidney biopsy remains the gold standard for diagnosis. Light microscopy (LM) demonstrates the typical crescent formation of RPGN (Figure 12-8). Immunofluorescence microscopy of a renal specimen distinguishes three major patterns of immunoglobulin deposition, representing three diagnostic categories:
What is the most likely diagnosis?
The man most likely suffers from renal artery stenosis. The bruit described is in the region of the renal artery; this finding, in addition to the sudden increase in blood pressure and hypokalemia supports the diagnosis of renal artery stenosis. Imaging confirms the diagnosis.
What is the pathogenesis of renal artery stenosis in this patient and how would it differ in a young woman?
In the elderly population, renal artery stenosis is seen more often in men and is mostly caused by atherosclerotic plaques (secondary to hypercholesterolemia). For younger patients, fibromuscular dysplasia of the renal arteries, seen more in females, would be the likely cause.
What changes in renin secretion from each kidney are likely in renal artery stenosis?
The kidney ipsilateral to the stenosis will increase renin secretion in response to a perceived decrease in arterial pressure due to decreased flow to the juxtaglomerular apparatus. The contralateral kidney will respond to the patient’s resulting hypertension by decreasing its renin secretion (Figure 12-9).
What is the most likely diagnosis?
Nephrolithiasis (kidney stones). Acute back/side pain (especially related to movement or that waxes and wanes) with elevated calcium and RBCs in the urine indicates kidney stones.
How is Nephrolithiasis classified?
Approximately 85% of renal calculi are calcium oxalate stones (Figure 12-10), which are strongly radiopaque. The second most common kid- ney stones are struvite (ammonium magnesium phosphate), which are radiopaque and associated with Proteus vulgaris and Staphylococcus aureus infection. Other, less common stones include uric acid stones (radiolucent) and cystine stones (moderately radiopaque). This patient most likely has calcium oxalate stones given her hypercalcemia and normal temperature.
How is Nephrolithiasis classified?
Approximately 85% of renal calculi are calcium oxalate stones (Figure 12-10), which are strongly radiopaque. The second most common kid- ney stones are struvite (ammonium magnesium phosphate), which are radiopaque and associated with Proteus vulgaris and Staphylococcus aureus infection. Other, less common stones include uric acid stones (radiolucent) and cystine stones (moderately radiopaque). This patient most likely has calcium oxalate stones given her hypercalcemia and normal temperature.
What is the most likely diagnosis?
Hyponatremia
In this case, what is the most likely etiology of the patient’s volume status?
This patient’s small cell lung tumor raises the likelihood of SIADH (a paraneoplastic syndrome for small cell lung cancer). Physical findings and lab values are also consistent with SIADH.
What is cross-matching?
In transplantation, the process of cross-matching determines whether the recipient has antibodies to the donor’s WBCs. This measure prevents hyper acute rejection due to preformed antibodies.
If CMV is present, what fraction of a blood sample will have the highest yield for the virus?
Because CMV invades WBCs, these cells contain the highest titer of the virus. Upon centrifuging a blood sample, a “buffy coat,” representing < 1% of blood and seen between the plasma and hematocrit, will separate out most of the WBCs and platelets. Figure 12-11 shows a CMV giant cell with multiple hyaline inclusions.
Why is CMV of particular concern in this patient?
The girl is immunosuppressed, and there is a significant probability that she has been exposed to CMV. Approximately 80% of normal adults are infected with CMV yet remain asymptomatic because of their functional immune systems. Therefore, there is a high likelihood that the donor may have been CMV positive. As with other members of the herpes virus family, CMV is more likely to activate in an immunosuppressed host. In the immunocompromised host CMV can cause a variety of syndromes, including a mildly febrile upper respiratory illness, severe gastrointestinal syndrome with mild hepatitis, marked pancytopenia, or pneumonitis. CMV can also directly cause graft dysfunction.
What is the most likely diagnosis?
This boy most likely has vesicoureteral reflux (VUR), which is the most common urologic finding in children. It is seen in 1% of all newborns and almost 50% of young children presenting with a UTI.
What is the innervation of the bladder?
