Renal system Flashcards
In the diagnosis of malignant renal hypertension, which of the following statements is correct?
A Due to kidney dysfunction, there is decreased levels of renin
B Occurs in 5-10% of individuals with an elevated blood pressure
C Malignant hypertension only occurs in patients with previous hypertension
D The morphology picture of onion skinning is proportional to the degree of renal failure
D
Explanation
Malignant hypertension is the form of renal disease associated with malignant or accelerated phase of hypertension. This pattern of hypertension may occasionally develop in normotensive individuals but is more often super imposed on pre-existing benign hypertension, secondary forms of hypertension or underlying chronic renal disease (glomerulonephritis or reflux nephropathy). It is an uncommon condition occurring in1 to 5% of patients with elevated blood pressure. Occurs more often in younger people and the black population.
The initial insult is some sort of vascular damage to the kidneys. This results in increased vessel permeability, focal death of cell walls and platelet deposition. This leads to fibrinoid necrosis of the arterioles and small arteries, swelling of the intima layer and vascular thrombosis. The kidneys become markedly ischaemic. With severe involvement of the afferent arteriole, the renin angiotensin system is activated. (Increasing the levels of plasmin renin dramatically)
The microscopic changes reflect the pathogenic events of malignant hypertension. There is intimal thickening caused by concentric proliferation of smooth muscle cells and collagen which accumulates in a layered configuration (together with accumulation of proteoglycans and plasma proteins). This gives an onion skinning appearance. This lesion is also called hyperplastic arteriolitis and correlates with renal failure in malignant hypertension
Regarding post infectious glomerulonephritis which of the following statements is correct?
A Most patients will develop renal failure
B Occurs 1- 4 weeks post impetigo
C Is due to the toxic effect of streptolysin on the basement membrane
D Is due to Group B alpha-haemolytic streptococcus
B
Explanation
Acute glomerulonephritis occurs most frequently in children aged 6-10yrs, 1-4 weeks after a streptococcal infection of the pharynx or skin (impetigo). It is due to a group A beta haemolytic streptococcus. The streptococcal antigenic component responsible for the immune reaction has eluded identification for years but most of the evidence suggests streptococcal pyogenic exotoxin B (SpeB). More than 95% of affected children will recover.
Note: impetigo is a skin infection caused by both Staphylococcus aureus (most commonly), and Streptococcus pyogenes
Which of the following is correct in relation to nephrotic syndrome?
A Mild proteinuria
B Albumin is lost, other globulins are unaffected
C There is alteration to serum lipid levels
D Decreased interstitial fluid volume
C
Explanation
The manifestations of nephrotic syndrome include: massive proteinuria, hypoalbuminemia, generalised oedema (increased interstitial fluid), hyperlipidaemia and lipiduria. Hypertension is present in 15-35% of cases.
Nephritic syndrome: haematuria, azotaemia, variable proteinuria, oliguria, oedema and hypertension
Note: hypertension can occur in both cases
Which of the following is not a nephrotoxic cause of acute tubular necrosis (ATN)?
A Lead
B Erythromycin
C Radiographic contrast material
D Aminoglycosides
B
Explanation
Causes of nephrotoxic ATN include: (from the textbook)
- Gentamicin
- Radiographic contrast agents
- Heavy metal poisoning
- Organic solvents
For interest: Regarding contrast and ATN.
The RANZCR position statement on the use of iodinated contrast media Recommendations.
The risk of intravenous contrast media related acute kidney injury (CI-AKI) is likely to be non-existent for patients with eGFR greater than 45 mL/min/1.73m2.
No special precautions are recommended in this group prior to or following intravenous administration of iodinated contrast media. R7.
The risk is of intravenous CI-AKI is also very likely to be low or non-existent for patients with eGFR 30 - 45 mL/min/1.73m2. Universal use of periprocedural hydration in this group to prevent the theoretical risk of CI-AKI cannot be recommended but patients with impaired function in this range that is acutely deteriorating rather than stable may benefit from this intervention.
In patients with severe renal function impairment (eGFR less than 30 ml/min/1.73m2) or actively deteriorating renal function (acute kidney injury) careful weighing of the risk versus the benefit of iodinated contrast media administration needs to be undertaken. Consideration should be given to periprocedural renal protection using intravenous hydration with 0.9% saline (see relevant section).
However, severe renal function impairment should not be regarded as an absolute contraindication to medically indicated iodinated contrast media administration. so perhaps contrast-induced nephropathy may be overstated.
Concerning acute tubular necrosis (ATN), which of the following statements is correct?
A ATN is the commonest cause of acute renal failiure
B Cephalosporins are not a causative agent
C Nephrotoxic causes are associated with a poor prognosis
D Rhabdomyolysis is not a cause
Renal failure can be caused by
A
Explanation
ATN
Organic vascular obstruction
Sever glomerular disease
Acute tubulointerstitial nephritis, most commonly due to hypersensitivity to drugs
Massive infection, pyelonephritis
DIC
Urinary obstruction
ATN
Systemic thrombosis/ embolism
DIC
Decreased effective circulating volume-hypovolaemic shock
Microangiopathies of the renal blood vessels
Endogenous agents (myoglobin, Hb, monoclonal light chains)
Exogenous agents (drugs, radiocontrast, heavy metals, solvents, antibiotics-gentamicin)
Other antibiotics are implicated. No examples are given in the textbook.
Web search-there are cases of cephalosporins causing nephrotoxic ATN (cephalexin, cephaloridine and cephalothin)
Nephrotoxin ATN has a better prognosis than ischaemic ATN.
Rhabdomyolysis releases nephrotoxin substances from damaged myocytes (myoglobin) and damaged myocytes sequester extracellular fluid provoking hypovolaemic decrease in renal perfusion.
ATN accounts for about 50% of cases of acute renal failure (the most commonest cause)
Drugs — Virtually any drug can cause AIN, although only a few have been reported with any frequency
The most common drug causes of AIN now include
Nonsteroidal anti-inflammatory agents (NSAIDs), including selective cyclooxygenase (COX)-2 inhibitors
Penicillins and cephalosporins
Rifampicin
Antimicrobial sulfonamides, including trimethoprim-sulfamethoxazole
Diuretics, including loop diuretics such as furosemide and thiazide-type diuretics
Ciprofloxacin and to a lesser degree, other quinolones
Cimetidine only rare cases have been described with other H-2 blockers such as ranitidine
Allopurinol
Proton pump inhibitors such as omeprazole
Indinavir
5-aminosalicylates eg, mesalamine
Regarding acute tubular necrosis (ATN), which of the following statements is correct?
A 80% are associated with anuria
B It is associated with hyperkalemia in recovery
C The non-oliguric form has a better recovery
D It is associated with ischaemic cortical cells
C
Explanation
ATN is associated with hypokalaemia in the recovery phase. The tubules are still damaged so large amounts of water, sodium and potassium are lost in the flood of urine. Up to 50% of patients may have non-oliguric ATN which is associated with high urine volumes. This type of ATN generally follows a more benign clinical course. Ischaemic ATN is associated with focal tubular epithelial necrosis. The straight portion of the proximal tubule and the ascending thick limb in the renal medulla are especially vulnerable. There is rupture of the basement membrane and occlusion of tubular lumen by casts. The lesion occurs in a skip like pattern along the nephron with large gaps in between. The 3 stages of ATN include: initiating stage, maintenance stage (decreased urine output) and a recovery stage.
Ischaemic tubular necrosis (ITN) is associated with which of the following?
A Predominantly PST and ascending loop of Henle necrosis
B A maintenance stage with polyuria
C Intact basement membranes
D Cast obstruction of the proximal tubule
A
Explanation
Ischaemic ATN is associated with focal tubular epithelial necrosis. The straight portion of the proximal tubule (PST) and the ascending thick limb in the renal medulla are especially vulnerable, but focal lesions may occur in the distal tubule, often in conjunction with casts.
Latest edition-Ischaemic ATI is characterised by lesions in the straight portion of the proximal tubule (PST) and the ascending thick limbs, but no segment of the proximal or distal tubule is spared.
In the toxic type extensive necrosis is present along the PST (proximal straight tubules) segments with many toxins. However the ascending loop of Henle and the DCT are also involved. In both types the lumens of the DCT and collecting ducts contain casts. There is rupture of the basement membrane and occlusion of tubular lumen by casts. The lesion occurs in a skip like pattern along the nephron with large gaps in between. The 3 stages of ATN include: initiating stage, maintenance stage (decreased urine output) and a recovery stage.
Initiating phase: slight decrease in urine volume with a slight rise in BUN
Maintenance phase: sustained decrese in urine output, salt and water overload, rising BUN, hyperK, metabolic acidosis and manifistations of uraemia
Recovery phase: steady increase in urne volume, loss of water, sodium and potassium.
ATN is associated with hyperkalaemia in the maintenance phase and hypokalaemia becomes a problem in the recovery phase.
Up to 50% of patients with ATN do not have oliguria and instead have increased urine volumes. This so called non- oliguric ATN which is associated with high urine volumes. This type of ATN generally follows a more benign clinical course and is associated particularly with nephrotoxins
Regarding the hepatorenal syndrome, which of the following statements is correct?
A It only occurs in kidneys with existing disease
B It is irreversible
C The kidney maintian the ability to concentrate urine
D Urine has a high sodium concentration
C
Explanation
In hepatorenal syndrome- there is an appearance of renal failure in patients with severe liver disease, in whom there are no intrinsic renal disturbances (no intrinsic morphological or functional cause). Kidney function promptly improves if hepatic failure is reversed. Pathophysiology appears to consist of decreased renal perfusion pressure, followed by renal vasoconstriction. Because the renal ability to concentrate urine is retained, oliguria with hyperosmolar urine devoid of proteins and low in sodium occurs.
Which of the folowing statments is correct regarding urolithiasis?
A Calcium is the major component in 35% of calculi
B Presence of hypercalcaemia implies renal insufficiency
C A patient with leukemia is likely to make cystine calculi
D Struvite stones are made up of magnesium-ammonium-phosphate
D
Explanation
Leukaemia causes uric acid stones due to the high cell turnover and resulting hyperuricaemia.
Hypercalcuria can be due to absorptive (gastrointestinal hyper absorption) or renal (intrinsic impairment of renal tubule reabsorption) impairments.
Calcium oxalate stones 70% Struvite stones 15% Uric acid stones 5-10% Cysteine stones 1%
Regarding pyelonephritis, which of the following statements is correct?
A Papillary necrosis and perinephric abscess are common seqelae
B 85% of infections are caused by Gram negative bacteria
C Ureteral obstruction makes haematogenous infection less likely
D Infection is less likely during pregnancy
B
Explanation
Infection is more likely in pregnancy. 4-6% of pregnant women have bacteruria and 20-40% will develop a symptomatic infection if not treated. Haematogenous infection is more likely to occur in the presence of ureteral obstruction, in debilitated patients and in patients receiving immunosuppressive therapy. It is associated with non-enteric organisms such as staphalococcus or fungi. Patchy interstitial suppurative inflammation and tubular necrosis are the hallmarks of acute pyelonephritis
Alkalinisation of urine may precipitate which of the following renal calculi?
A Cystine stones
B Calcium oxalate stones
C Uric acid stones
D Struvite stones
D
Explanation
Uric acid stones form in acid urine- pH<5.5. If the urine is alkaline, uric acid remians soluble and does not precipitate out. This forms the basis of treatment of uric acid calculi. Struvite stones develop when the pH is higher than 7.2 and ammonia is present in the urine. Calcium stones-calcium oxalate develops in acid urine and calcium phosphate develops in alkaline urine (pH >7.2). Cystine stones are caused by genetic defects in the renal reabsorption of aminoacids, including cystine, leading to cytinuria. Stones form at low urinary pH.
Which of the following statements is true about adult polycystic kidney disease (PKD)?
A It is an autosomal recessive disease
B Mitral valvular disease is present in 20 - 25% of patients
C Most die from a ruptured berry aneurysm
D It can cause chronic renal failure in 2% of affected patients
B
Explanation
APKD is an autosomal dominant (adult) kidney disease. It is relatively common affecting 1 of every 400-1000 live births. It accounts for 5-10% of cases of Chronic Renal Failure (CRF) requiring transplantation or dialysis. Extra-renal congenital abnormalities are common, 40% have polycystic liver disease. Intracranial berry aneurysms arise in the circle of Willis and Sub-arachnoid Haemorrhage (SAH) account for 4-10% of individuals. Mitral valve prolapse and other cardiac valvular anomalies occur in 20-25% of patients, but most are asymptomatic. Ultimately about 40% of adult patients die of coronary or hypertensive heart disease, 25% of infection, 15% of ruptured berry aneurysms or hypertensive intracerebral bleed.
Note: there is a form of autosomal recessive (childhood) polycystic kidney disease which is genetically distinct from adult PKD
PKD1 mutation causes CRF in 95% of patients by age 70 PKD2 mutation causes CRF in 45% of patients by age 70 Either way.
Therefore, adult PKD is autosomal dominant and not recessive, making the statement: It is an autosomal recessive disease-wrong
Extra:
Autosomal recessive polycystic kidney disease (ARPKD) is a rare genetic disorder occurring in approximately 1 in 25,000 children, equally affecting boys and girls. While ARPKD can cause death in the first month of life, almost 80% of ARPKD children survive the newborn period. Past that, one-third will need a transplant or dialysis in the first 10 years.
The prognosis for ARPKD has changed dramatically—it’s no longer considered a fatal condition. Twenty years ago, only half of the children born with the disease survived to their 10th birthday. Now, more than 90% of children who survive the newborn period reach their 20th birthday and 50% of these survivors do not yet require dialysis or a transplant. Autosomal Recessive Polycystic Kidney Disease (ARPKD): This is a less common type of PKD. It is caused by mutations in the PKHD1 gene and typically presents in infancy or early childhood. ARPKD is more severe than ADPKD, often leading to kidney failure in childhood.
A 5yr old girl presents to the emergency department with malaise, fever, nausea, oliguria and haematuria. You identify red cell casts in her urine. What is the most likely diagnosis?
A Membranous glomerulopathy
B Post streptococcal glomerulonephritis
C Focal, segmental glomerulonephritis
D Minimal change disease
B
Explanation
Poststerptococcal glomerulonephritis usually appears 1-4 weeks after a streptococcal throat or skin infection. It occurs most frequently in ages 6-10yrs, but adults of any age can be affected. The A beta haemolytic streptococci are the causative agents, but only certain strains are nephrogenic. More than 90% of cases being traced to types 12, 4 and 1.
It is an immune mediated disease-type III hypersensitivity reaction.
Clinical picture: abrupt malaise, fever, nausea, oliguria and haematuria 1-2 weeks after recovery form a sore throat. The patients have red cell casts in the urine, mild proteinuria (<1gm/day), periorbital oedema and mild to moderate hypertension. More than 95% of cases eventually recover with only conservative therapy of maintaining a salt and water balance. Few progress to a chronic glomerulonephritis with or without recurrence of an active nephritic picture. Adults present more atypically with the sudden appearance of hypertension., oedema with the elevation of the renal urea and creatinine.
Minimal change disease is associated with children, but it typically does NOT present with haematuria.
What is the most common cause of chronic pyelonephritis?
A Pregnancy
B Chronic vesicoureteral reflux
C Chronic obstructive pyelonephritis
D Chronic catheterisation
B
Explanation
Chronic pyelonephritis is a disorder in which chronic tubulointerstitial inflammation and scarring are associated with pathological involvement of the calyces and pelvis. Chronic pyelonephritis is an important cause of end stage chronic kidney disease. This condition remains an important cause of kidney destruction in children with severe lower urinary tract abnormalities
Chronic pyelonephritis can be divided into two forms
Chronic reflux nephropathy-more common
Chronic obstructive pyelonephritis
Note: both conditions can result in bilateral pyelonephritis. Vesicoureteral reflux occurs in 1-2% of otherwise normal children
How long does it usually take for a post streptococcal of the pharynx to develop glomerulonephritis?
A 6 months
B 2 weeks
C 5 days
D 3 months
B
Explanation
Post streptococcal glomerulonephritis usually appears 1-4 weeks after a pharyngeal or skin infection (impetigo). PSG occurs most frequently in children aged 6-10yrs, but adults of any age can be affected.
Post-streptococcal glomerulonephritis can occur after pharyngeal infection. What is the usual time period between events?
A 13-16 weeks
B 1-4 weeks
C 5-8 weeks
D 9-12 weeks
B
Which type of hypersensitivity reaction underlies the pathological changes seen in post-streptococcal glomerulonephritis?
A IV
B I
C II
D III
D
Explanation
Post-streptococcal GN is due to formation and deposition of antigen-antibody complexes in tissues causing subsequent tissue damage.
What is the usual causative organism in post-streptococcal glomerulonephritis?
A E. Coli
B Group A Streptococcus
C Group B Streptococcus
D S. aureus
B
An elderly man presents with epididymo-orchitis. What is the most likely pathogen?
A S. faecalis
B E.coli
C C.trachomatis
D N.gonorrhoeae
B
Explanation
In sexually active men younger than age 35 years: Chlamydia trachomatis and Neisseria gonorrhoeae are the most frequent culprits.
In men older than 35, the most common urinary tract pathogens such as E. coli and Pseudomonas are responsible for most infections
