Renal Flashcards
What is a normal GFR?
100 mL/min
What is used to estimate RPF?
PAH clearance
What is a normal Na+ and K+ level in the blood?
Na+= 135-145 K+= 3.5-5
What is a normal BUN, Cr, and BUN/ Cr ratio?
BUN= 7-20 Cr= 0.6-1.2 BUN:Cr= 15:1
What is normal CO2, bicarbonate, and pH of the blood?
CO2= about 40 HCO3- = about 24 PH= 7.35-7.45
What is a normal level of albumin in the blood?
3.5-5.5
What does natriuresis mean?
Excretion of Na+ in the urine
What does “oliguria” mean?
Low urine output
Which germ layer do kidneys develop from in embryo?
The mesoderm
What are the 3 names for the stages of the developing kidney?
1) pronephros (degenerates)
2) mesonephros (degenerates)
3) metanephros (becomes adult kidney)
What does the ureteric bud form in embryo?
The collecting system (ureter, pelvises, calyces) and collecting duct
What does the metanephric mesenchyme form in embryo?
All parts of the nephron except the collecting duct (the ureteric bud forms this)
What is unilateral renal angenesis?
You don’t have 1 of your kidneys
The ureteric bud (which forms the collecting system and collecting duct) fails to form—> no signals sent to metanephric mesenchyme for it to differentiate (and form all the parts of the nephron except the CD)—> you get complete abscence of a kidney + ureter
What is multicystic dysplastic kidney?
When the ureteric bud forms, but does not send the signals to stimulate differentiation of the metanephric mesenchyme—> one kidney is unfunctional like a cyst
What is vesicoureteral reflux?
When there is backflow of urine from the bladder up to the kidneys. Results from abnormal insertion of the ureters into the bladder. (Associated with duplex ureters)
What is a duplex collecting system? What conditions is it associated with.
A congenital problem where the baby has 2 ureters on one side (and just 1 like normal on the other side). Due to bifurcation of the ureteric bud (which forms the ureters) before it enters the metanephric blastema.
Strongly associated with vesicoureteral reflux (backflow of urine from ureters up to kidneys) bc if the ureters form abnormally, they often insert abnormally. Also associated with urethral obstruction. Increases risk for UTIs.
Describe Potter syndrome.
Collection of symptoms due to dec amniotic fluid.
Baby has a kidney problem: autosomal recessive Polycystic kidney disease (ARPKD), obstructive uropahty, bilateral renal agenesis (kidneys don’t form on either side), or chronic placental insufficiency—> not peeing—> dec amniotic fluid (oligohydraminos)—> smushed face, limb deformities, pulmonary hypoplasia (underdeveloped lungs bc baby swallows amniotic fluid to expand and further develop lungs) and death.
Mnemonic: “POTTER” Pulmonary hypoplasia, Oligohydramnios (trigger), Twisted face, Twisted skin, Extremity defects, Renal Failure (in utero).
What is posterior urethral valves?
Congenital defect in baby boys. A tissue flap obstructs urine outflow from the bladder—> urine builds up in the kidneys (hydronephrosis).
*this is the most common cause of bladder obstruction in male infants.
A baby boy has a bladder obstruction. What is the most likely cause?
Posterior Urethral Valves.
Congenital defect in baby boys. A tissue flap obstructs urine outflow from the bladder—> urine builds up in the kidneys (hydronephrosis).
*this is the most common cause of bladder obstruction in male infants.
What is “horseshoe kidney?”
When the inferior parts of the 2 kidneys are linked together—> kidneys cannot ascend in the pelvis like they normally do during development so they stay lower in the pelvis (they get stuck below the INFERIOR MESENTERIC ARTERY).
Which congenital abnormality of the kidneys is associated with Turner syndrome?
Horseshoe kidney
What is the urachus?
Embryolical structure that connects the dome of the bladder to the umbilicus. This is obliterated at birth—> median umbilical ligament.
An adult has painless hematuria (common sign of bladder CA) and cancer is found at dome of bladder. Pathology shows it is adenocarcinoma. Where did this come from?
The embryological structure: the urachus.
Urachal remnants can lead to adenocarcinoma of the bladder
If the urachus fails to obliterate at birth, what will be seen?
Urine leaking from the belly button (bc the urachus connects the dome of the bladder to the umbilicus…normally goes away before birth and becomes the median umbilical ligament).
What is hydronephrosis?
Increased fluid in the kidney from back up (for example, if there is bladder obstruction and urine cannot get out to go down through ureters, the urine will stay behind in the kidneys)
What’s the difference between central and nephrogenic diabetes insipidous?
Central DI- not producing ADH
Nephrogenic DI- not responding to ADH
Which types of kidney stones are more likely to precipitate/ form with acidic pH urine? What about with alkaline urine?
Precipitates with low pH (acidic) urine—> Uric acid stones AND cystine stones
Precipitates with high pH (alkaline) urine—> Calcium phosphate stones AND ammonium magnesium phosphate (struvite) stones
What is tumor lysis syndrome and how does it relate to kidney stone formation?
Tumor lysis syndrome= complication of chemo where a bunch of cells are killed at the same time and release their contents like K+, phosphorous, and uric acid into the bloodstream.
This will increase risk for development of kidney stones (for example, uric acid stone—so hydrate and alkalize urine to prevent this type).
Which segments of the nephron have the lowest pH (most acidic/ most H+)?
The DCT and CD
What are the 4 CAUSES of the Potter sequence?
Autosomal recessive polycystic kidney disease (ARPKD), obstructive uropathy (ex: posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency
What affect will a beta-blocker have on renin, ATI, ATII, Aldosterone, and Bradykinin?
A beta-blocker will DECREASE renin, ATI, ATII, Aldosterone (because it inhibits renin, and everything else is downstream from that) and will NOT CHANGE bradykinin levels (only ACE is involved with bradykinin breakdown).
Why can a beta-blocker be used to treat hypertension?
The beta-1 receptor on the kidneys increases renin release. This is one of the receptors a beta-blocker will inhibit—> decreased renin release—> dec ATI—> dec ATII—> dec Aldosterone (dec Na+ reabsorption)—> dec BP.
What is the inheritance pattern of cystic fibrosis (CF)?
Autosomal recessive.
Explain altitude sickness. What drug can help it and why?
High altitude (hypoxia= dec oxygen)—> hyperventilation (blow off more CO2)—> dec CO2= metabolic alkalosis. Kidneys will compensate by dec bicarbonate reabsorption and H+ secretion (we want less bicarb in the blood and more H+ to stay in blood to compensate with a metabolic acidosis over days). RBCs will also increase their molecule 2,3-BPG, which stimulates Hb to unload oxygen and deliver it to tissues. Acetazolamide (Carbonic Anhydrase Inhibitor) can help the body compensate faster (and thus reduce altitude sickness symptoms) by dec bicarb reabsorption.
What’s the difference between central and nephrogenic diabetes insipidous (DI)?
Central DI- you’re not making ADH
Nephrogenic DI- you’re not responding to ADH
(Pee more: body is more concentrated, urine is more dilute)
What is the equation to estimate RPF (renal plasma flow)? What is the equation to calculate RBF (renal blood flow)?
RPF can be estimated by the clearance of PAH.
RPF= Cl of PAH= ([PAH]in urine * V)/ [PAH]in blood, where V= urine volume flow rate
RBF= RPF/ (1-hematocrit)
What triad of symptoms may be seen in Renal Cell Carcinoma (RCC)? Pathogenesis involves loss of what tumor suppressor gene?
Hematuria (peeing out blood), palpable mass, and flank pain (*though often all 3 aren’t seen together).
Loss of VHL (3p) tumor suppressor gene
Drugs that end in “-sartan” are what kind of drugs?
ARBs (angiotensin II receptor blockers)
You have a patient on a beta-blocker to manage his/her HTN. They hate it because they are coughing a lot. What medication can you switch them to?
an ARB (angiotensin II receptor blocker) *ARBs do the same thing as ACE inhibitors (block the RAAS from elevating BP, etc.) but don’t come along with cough and angioedema as side effects since not involved with Bradykinin. ARBs just aren’t quite as good, so we usually prescribe an ACE inhibitor first.
What is hydronephrosis?
Dilation of renal pelvis and calyces. Usually caused by urinary tract obstruction (ex: renal stones, severe BPH, cervical CA, injury to ureter). Other causes include retroperitoneal fibrosis, vesicoureteral reflux.
You’re in metabolic acidosis. How will the lungs immediately compensate? What will the kidneys try to do (3 things) to try to compensate?
Metabolic acidosis= low bicarb.
The lungs will dec CO2 (hyperventilate) to compensate.
The kidneys will: (1) reabsorb more bicarb in the PCT (you have low bicarb so you need to push more into the blood to increase it back to normal), (2) increases H+ secretion throughout the nephron (you have acidosis so you want to pee out more acid), (3) makes more buffer (HPO4(2-) and NH3) so that H+ can be secreted w/o changing the pH of the urine by too much.
What is the detrusor muscle?
Muscle that forms the wall of the bladder. (It is the bladder muscle NOT the pelvic floor muscle)
What is nephrotic syndrome? Explain generally what the problem is and key findings.
Damage to podocytes (from primary cause meaning direct sclerosis or from secondary cause like DM)—> disruption of glomerular charge barrier—> proteins can get through (they shouldn’t be able to)—> pee out a lot of protein (>3.5 g/day)—> less protein left behind in blood (hypoalbuminemia)—> edema (due to less oncotic pressure) and hyperlipidemia (lost protein in blood= thin blood so liver throws excess fat into it to “bulk it up”).
You also see “frothy urine” (from the protein) with fatty casts.
Nephrotic syndrome can cause hypercoagulation due to antithrombin (AT) III lost in urine (AT is a protein that stops coagulation, so if you pee it out—> too much clotting) and inc risk of infection due to loss of immunoglobulins in urine.
What is nephritic syndrome? Explain generally what the problem is and key findings.
Inflammatory process (the damage doesn’t extend to the charge barrier, or else it’d be nephrotic). You get blood in urine (hematuria) and RBC casts in urine. Associated with azotemia (inc nitrogen waste products in blood), oliguria (dec urine output), hypertension (they retain salt for some reason), and proteinuria (but don’t pee out as much protein as in nephrotic syndrome).
What does “frothy urine” often indicate and why?
Nephrotic syndrome.
Bc you are peeing out a lot of protein (and protein in a liquid makes it “frothy”…just like if you dump a bunch of protein powder into bottled water it will kinda fizz up).
A positive bladder stress test (directly observed leakage from urethra upon coughing or Valsava maneuver/ bearing down) is diagnostic of what type of urinary incontinence?
Stress incontinence (weakened pelvic floor muscles—> urethral sphincter dysfunction—> leakage of urine when you inc abdominal pressure from coughing, sneezing, etc.)
A diabetic patient is having trouble fully emptying his bladder and is having dribbling of urine throughout the day. What type of urinary incontinence is this and how is it caused in this patient?
Overflow incontinence. Diabetic neropathy—> nerves damaged/ not working well to contract the detrusor (bladder) muscle—> incomplete emptying of bladder—> leakage of urine throughout the day, not just from coughing or sneezing.
What are the 3 types of urinary incontinece? What are they caused by and what’s the main symptom?
1) STRESS INCONTINENCE- weakened pelvic floor muscles (from being obese, post-delivery, post-GU surgery, etc.)—> urethral sphincter dysfunction—> leakage of urine when you inc abdominal pressure (cough, sneeze, bear down)
2) URGENCY INCONTINENCE- irritation or hyperreflexia (neurological or psychological)—> overactive bladder/ detrusor hyperactivity—> sudden, strong urge to void urine and you might not make it to the bathroom w/o dribbling
3) OVERFLOW INCONTINENCE- detrusor (bladder) muscle underactivity (such as from diabetic neropathy—> nerves not working to contract the detrusor muscle) or outlet obstruction (ex: BPH)—> incomplete emptying of bladder—> bladder builds up pressure and you get continuous leakage of a little urine throughout the day when the bladder pressure just overcomes the sphincter
What is the urachus? What is it a remnant of? What does it normally become once a baby is born? If this fails, what happens?
The urachus connects the dome of the bladder to the umbilicus. It is a remnant of the allantois, which connects the bladder and the yolk sac during fetal development. It normally obliterates (goes away) and becomes the median umbilical ligament. (If it fails to obliterate, urine can leak out from the belly button and inc risk for adenocarcinoma of the bladder.)
What’s one clue you can use to go “it’s nephritic, not nephrotic”?
Peeing out blood
Lung + kidney problems going on. What do you need to consider as a possible diagnosis?
Goodpastures syndrome!
When you pee, what happens to the bladder detrusor muscle? What happens to the urethral sphincters? (Do they contract or relax?)
The bladder (detrusor muscle) will contract to allow urination to happen. The urethral sphincters will relax.
**note: the pelvic floor muscle is on the same plane as the external urethral sphincter.
In multiple myeloma, what happens to the following levels? Ca2+ in blood, PTH, Renal Ca2+ reabsorption, Ca2+ in the urine, and vitamin D synthesis.
tumor related cytokines (esp IL-6)—> bone breakdown—> inc Ca2+ in the blood—> dec PTH (you don’t want a lot of PTH telling the body to inc Ca2+ in the blood since levels are already high)—> dec renal Ca2+ reabsorption (kidneys push less Ca2+ into the blood bc levels are already high)—> inc Ca2+ in urine (pee out more Ca2+ to compensate for high levels in the blood). Dec vitamin D synthesis (vitamin D helps with Ca2+ absorption from gut into blood, so you want less since levels are already high in the blood).
What does “contraction alkalosis” mean?
Alkalosis due to hypovolumia (loss of fluid)
You give an ARB. What happens to the levels of Renin, ATI, ATII, Aldosterone, and Bradykinin? (Increase, decrease, or stay the same)
ARB—> inc renin, ATI, ATII (ARBs= Angiotensin Receptors Blockers= block ATII from binding, so everything downstream/ after ATII will decrease, but everything before builds up)
Dec Aldosterone
No change to Bradykinin (only ACE inhibitors will dec Bradykinin, since ACE is involved in its breakdown)
Urine flows backward from bladder to ureters toward kidneys. What is this called?
Vesicoureteral reflux
Where are the ureters positioned in relation to the uterine artery (females) and vas deferens (males)? What application does this have if a woman gets a surgery involving ligation of the uterine or ovarian vessels?
Ureters pass under the uterine artery (females)/ vas deferens (males). “Water under the bridge.” Gynecologic procedures such as ligation of the uterine or ovarian vessels may damage the ureters—> urethral obstruction or leakage.
What do the juxtaglomerular cells do?
Secrete Renin.
What is the macula densa? Explain tubuloglomerular feedback.
Macula densa= specialized epithelial cells of the DCT (distal convoluted tubule). They sense delivery of NaCl to the DCT. If high GFR—> high NaCl delivery to the macula densa in the DCT—> it responds by causing constriction of the afferent arteriole to dec GFR back to normal to maintain homeostasis.
What are the relative concentrations of K+ and Na+ inside the cell? Outside the cell? (High or low)
High [K+] inside the cell, low [K+] outside the cell. “HIKIN’: HIgh K+ INtracellularly”
High [Na+] outside the cell, low [Na+] inside the cell. “In n’ Out: Na+ OUT”
What is the 60:40:20 rule?
60% TBW (total body water)—60% of your body weight is made up of water. Of that total, 40% (2/3rds) is in the ICF (intracellular space) inside of cells and 20% (1/3rd) is in the ECF (extracellular space) outside of cells. The ECF includes plasma and intrastitial fluid.
If clearance of X is less than GFR what does that mean? If it is greater than GFR what does that mean? If equal, what does that mean?
Cl < GFR (you’re clearing/ peeing out less than what you filtered through to begin with)—> net reabsorption
Cl > GFR (you’re clearing out more than what you filtered through)—> net secretion
Cl = GFR—> no net secretion or reabsorption
What is the equation for Fe(Na), or the fraction of excreted Na+?
Fe(Na)= ([Na]urine/ [Na]plasma) / ([Cr]urine/ [Cr]plasma)
Why does diabetes cause glucosuria (glucose in the urine)? At what point (put a number on it) do you start peeing out glucose?
Glucose at the normal plasma level (60-120 mg/dL) is completely reabsorbed in the PCT by Na+/glucose cotransport. But at 200 mg/dL (excess sugar in your blood), you start peeing out some glucose because you overwhelm the transporters. (*At RATE of 375 mg/min the transporters are all fully saturated, which is your Tm= transport max).
Which segment of the nephron contains a brush border?
The PCT (proximal convoluted tubule). This is the site that reabsorbs almost everything…all glucose and amino acids. Most (at least 65%) of bicarb, Na+, Cl-, PO4(3-), K+, water, and uric acid.
Angiotensin II (ATII) acts on which segment of the nephron to reabsorb Na+ (and thus inc BP)?
The PCT (proximal convoluted tubule).
Carbonic anhydrase inhibitors (Acetazolamide) act on which segment of the nephron?
The PCT (proximal convoluted tubule).
Loop diuretics act on which segment of the nephron?
The thick ascending loop of Henle.
Thiazide diuretics act on what segment of the nephron?
The early DCT (distal convoluted tubule).
K+ sparing diuretics act on what segment of the nephron?
The CD (collecting duct).
What is anemia of chronic kidney disease (CDK)?
Lack of EPO due to failing kidneys.
Kidneys make EPO, which stimulates the bone marrow to produce RBCs. When the kidneys aren’t working, it stops producing sufficient EPO—> patients can develop anemia!
Poorly controlled diabetic patient comes in with high serum Creatinine and BUN levels, low GFR. Also complains of being tired all the time and has low Hb. What’s going on?
Probably diabetes—> diabetic nephropathy (renal damage secondary to the diabetes)—> anemia of chronic kidney disease (CKD) (anemia secondary to the kidney damage bc kidneys secrete EPO, so if they aren’t working they don’t secrete adequate EPO to stimulate the bone marrow to make RBCs—> low RBC count!)
You are dehydrated. Which part of the nephron is the most dilute? Which part of the nephron is the most concentrated?
When you are dehydrated, ADH is activated in the collecting duct (CD) (ADH binds to V2 vasopressin/ ADH receptors on the CD—> aquaporin insertion—> reabsorption of more water—> you retain more water, pee out less water). So, the CD will be the most dilute part of the nephron (it reabsorbed a bunch of water, so only has the concentrated stuff in its tubule) and the thick ascending loop of Henle and DCT are the most concentrated parts (they are the last parts before the CD—before the water gets pulled out from the concentrated stuff to get reabsorbed).
If you clamp off the renal artery (like renal artery stenosis), how will the juxtaglomerular apparatus (JGA) of the kidney respond? Be specific about what cells are involved in this response.
Clamped down/ stenotic renal artery—> kidney—specifically the macula densa= specialized epithelial cells of the DCT—read/ sense low BP. The juxtaglomerular cells= specialized smooth muscle cells in the wall of the afferent arteriole secrete Renin in response to drive up BP. *Over a long time of poor perfusion to the kidneys, the JGA cells can undergo hyperplasia.
What diuretic has a side effect of gynecomastia (male breasts) due to its anti-androgen effects?
Spironolactone
What Ca2+ lab values (blood and urine) are you most likely to see in a patient with calcium oxalate or calcium phosphate kidney stones?
Normocalcemic (normal Ca2+ levels in blood) and hypercalciuria (high Ca2+ levels in the urine). Although hypercalcemia (high Ca2+ levels in blood) can lead to high Ca2+ in urine—> Ca2+ kidney stones, more commonly people with these stones have normal Ca2+ levels in blood because of regulation from Vit D and PTH (unless they have an underlying metabolic disorder). The Ca2+ in their urine is just high and it’s idiopathic (but could be due to inc GI absorption of Ca2+, inc mobilization of Ca from bone, or dec renal tubular Ca2+ reabsorption).
How can diabetes lead into urinary incontinence? How about anemia?
Diabetic neropathy (messes up nerves)—> nerves not working well to contract bladder (by the detrusor muscle)—> incomplete emptying of bladder—> inc pressure in bladder—> leakage of urine throughout the day when pressure in bladder overcomes sphincter (this is overflow urinary incontinece)
Diabetic nephrophaty (messes up kidneys)—> kidneys normally secrete EPO to stimulate the bone marrow to make RBCs, so if they aren’t working you don’t get all this EPO—> low RBC count= anemia of chronic kidney disease (CKD) secondary to diabetes
Where is aldosterone secreted from?
The adrenal glands (on top of the kidneys)
What is Conn’s syndrome?
Disease of the adrenal glands (on top of the kidneys)—> excess aldosterone production
What will aldosterone do to the BP, K+ levels in the blood, pH levels of the blood, and renin levels secreted by the kidney (juxtaglomerular cells)?
Aldosterone (reabsorbs Na+ and secretes K+ and H+ in the CD)—> high BP (from hypernatremia, or high Na+ in the blood), hypokalemia (low K+ bc you pee it out), alkalosis (low H+ bc you pee it out), less renin release (negative feedback, the kidneys don’t want to secrete more renin to drive up BP when BP is already high from aldosterone release)
What cause of Acute Tubular Necrosis (ATN) (intrinsic Acute Kidney Injury, or AKI) is associated with oxalate crystals in urine?
Ethylene glycol poisoning
(*also associated with AG metabolic acidosis, altered mental status, vacuolar degeneration, and ballooning of the proximal tubular cells)
Kid has a defective transporter in the gut and PCT of the kidneys that impairs absorption of Cysteine, Ornithine, Lysine, and Arginine. What is this condition called? What is the inheritance pattern of this condition? What kidney infections is the kid at risk for having recurrently? What will the urine crystals look like?
Cystinurea (defective amino acid transporter in the gut and PCT of kidneys, decreasing the reabsorption of “COLA”: Cysteine, Ornithine, Lysine, and Arginine). Autosomal recessive. Cysteine kidney stones. Hexagonal (“SIXtine stones have SIX sides”).
How do loop and Thiazide diuretics cause hypokalemia and alkalosis as side effects?
Loop and Thiazide diuretics are the strongest diuretics. They are blocking Na+ reabsorption so that you will pee out more Na+ (and therefore water) and get rid of excess fluid. So…since they block a lot of Na+ from being reabsorbed in earlier parts of the nephron (asc loop of Henle and DCT), they increase Na+ delivery to the CD. The CD responds to this excess Na+ it is receiving by increasing aldosterone (RAAS), which will work to reabsorb more Na+ and will also dump out more K+ and H+ in the urine since it acts on those 3 channels—> hypokalemia and alkalemia.
**seems counterintuitive that the diuretic is given to block Na+ reabsorption, but the CD of the kidney nephrons will respond to that by reabsorbing more Na+ (with the help of aldosterone). But, remember that the CD is for fine-tuning. So no matter how hard the CD tries to reabsorb that extra Na+, it won’t reabsorb too much of it and the diuretic will still have it’s desired effect!!
Post-strep GN is what type hypersensitivity reaction?
Type III (antibody-antigen complexes, circulating antibodies bound to strep antigen, deposit in kidney glomerulus)
What does “sterile pyuria” mean and what is it suggestive of?
Urine that has WBCs but appears to have no bacteria, so not a UTI. Suggestive of Chlamydia or Gonorrhea (in these STD’s the patient does have both WBCs and bacteria in their urine, but only the WBCs can be detected bc Chlamydia/ Gonorrhea don’t have cell walls that can be cultured so it’s “sterile pyuira”)
What are WBC casts?
WBCs that have formed into the shape of the renal tubules from passage down the tubules. Suggestive of a kidney infection (pyelonephritis).
What is Fanconi syndrome? What pH disorder does it come along with?
Your PCT (proximal convoluted tubule) is not working (it is a generalized reabsorptive defect in the PCT). Since the PCT normally reabsorbs a lot of stuff, you get lack of reabsorption—> pee out a lot more stuff than you should (nearly all glucose, amino acids, bicarb, PO4(3-), etc.). You get metabolic acidosis bc you pee out bicarb rather than reabsorbing 85% of it into the bloodstream at the PCT (pee out bicarb= less bicarb in blood= metabolic acidosis).
Barter syndrome has the same effect as _____diuretics. Gitelman syndrome has the same effect as _____diuretics. What inheritance pattern do both have?
Bartter syndrome= loop diuretics
Gitelman syndrome= Thiazide diuretics
(My mnemonic: “Bart is loopy.” And “gentleman (sounds like gitelman) say thank you (th is for Thiazide))
Both are AUTOSOMAL RECESSIVE.
What renal tubular defect resulting from a gain-of-function mutation presents like hyperaldosteronism, but levels of aldosterone are actually really low? Explain. What’s its inheritance pattern? What can you treat this condition with?
Liddle syndrome. Autosomal dominant.
This is a gain-of-function mutation where you have excess Na+ reabsorption in the CD (collecting duct) as if this channel is being overstimulated or like if aldosterone is released. Just like the effects of aldosterone, in this condition you get more Na+ going into blood—> high BP and more K+ and H+ going into the tubules to get peed out= less in blood—> hypokalemia and metabolic alkalosis. Levels of aldosterone are undetectable due to negative feedback.
Treat with Amiloride (K+ sparing diuretic that will block the Na+ channels in the CD).
Patient comes in with a pH of 7.25, CO2 of 70, and bicarb of 25. Is it more likely that he has COPD or overdosing on Heroin?
More likely he’s overdosing on Heroin.
Why? He has a low pH (acidosis) and high CO2 (respiratory). The kidneys compensate for this by increasing bicarb reabsorption. But, this is a slow-ish compensation (kidneys take 3-5 days to do this), so you won’t see a big increase in the bicarb until then. In other words, if it’s an acute-onset respiratory acidosis, we won’t see much change in bicarb (this is the case of this patient who has a bicarb of 25, pretty much normal, and Heroin overdose is an acute problem). If it were a chronic respiratory acidosis like COPD, the bicarb would be higher (the kidneys have had time to compensate).
*Heroin causes respiratory acidosis due to hypoventilation. COPD due to air/ CO2 trapping bc it’s hard to get air out in obstructive lung dz.
What does “postcoidal bleeding” mean?
Bleeding after having sex
How does ureter obstruction affect GFR?
Will decrease it.
Blockage after the kidneys—> backing up of urine/ fluid into the kidneys (hydronephrosis) which inc hydrostatic pressure—> GFR will decrease (if the kidneys are already full, they won’t want to filter through more and push in more fluid…the macula dense will sense extra NaCl delivery to the DCT and will respond by causing constriction of the afferent arteriole to reduce GFR)
What type hypersensitivity reaction is post-strep GN?
Type III (antibody-antigen COMPLEXES deposit into glomerulus).
Does second-hand smoke increase an infant’s risk for SIDS (sudden infant death syndrome)?
Yes! In fact, about half of SIDS cases involve smoker parents and second-hand smoke. This is most likely due to impaired arousal and cardiovascular responses.
What is Conn’s syndrome?
Primary hyperaldosteronism (the adrenal gland above the kidneys is pumping out way too much aldosterone)
*Renin levels are decreased in this case due to negative feedback and the RAAS is not in overdrive- just the adrenal glands, which are responsible for aldosterone release
During hypovolumic shock, why would the kidneys increase urea reabsorption?
Increasing urea reabsorption—> make a bigger concentration gradient in the interstitium—> more water drawn out/ reabsorbed in the thin descending loop of Henle, which is good (you want to retain fluid when you have a low BP)
In acute tubular necrosis (ATN), there are 3 phases: (1) the event, (2) maintenance phase, and (3) recovery phase. What ion disturbances are most likely to occur in the maintenance phase? Recovery phase?
Maintenance phase—> hyperkalemia and metabolic acidosis (can’t pee—> can’t excrete K+ and H+)
Recovery phase—> hypOkalemia (tubule cells regain function quickly, within 1-3 weeks, and you waste K+)
Crescent formation with liner IgG deposits seen on biopsy of a kidney. What is this?
Goodpastures
(“Crescent formation” means it’s Rapidly Progressive GN (RPGN) and “linear IgG deposits” means specifically Goodpastures bc it is antibodies against the type 4 collagen in BM, which is everywhere in the glomerulus so the antibodies line up and affect everywhere—> liner IF)
Teenager had the flu and 5 days later got blood in urine, slight edema. No family history of lung or kidney disease. This has happened twice now. Most likely diagnosis?
IgA neropathy (Berger’s dz)
Happens around 5 days after URI (like the flu) and can be recurrent. In teens/ young adults. Nephritic syndrome with IgA deposits in mesangium.
Guy has a thrombus in his right common femoral artery. Removal of the thrombus—> elevated creatinine kinase levels. Why?
This is an example of re-perfusion injury (due to oxygen free-radical generation, mitochondrial damage, and inflammation). Damaged cells leak out creatinine kinase, so this level will be elevated in patients with re-perfusion injury (that’s the risk we take when we give an ischemic patient back blood flow, but of course, it’s necessary).
Diabetic patient is taking diuretics and you added ACE inhibitor on top of that to protect her kidneys (since mild blood in urine was found, and you want to protect against diabetic nephropathy). What side effect may be a problem with this treatment plan?
Hypotension, even syncope. Diuretics dec BP and an ACE inhibitor on top of that will dec BP further and take away the RAAS ability to compensate.
Is giving prophylactic antibiotics helpful in reducing the likelihood a UTI will develop when giving a patient a urinary catheter?
No. The best way to prevent UTI is by removing the catheter as soon as it is no longer needed!
Girl presents with HTN and sometimes has episodes of fever and abdominal pain. Other than that, she has no symptoms and no family history of kidney disease. Renal ultrasound shows dilated renal calyces and overlaying renal scarring in the upper and lower poles. Most likely diagnosis?
Vesicouretal reflux
Retrograde flow of infected urine from bladder up through ureters—> pyelonephrosis/ kidney infections
What are the risk factors for bladder cancer?
Smoking and occupational exposure.
More detailed answer…
Main one is smoking. Also occupational exposure (to azo dyes—like hair cutters—and to naphthylamine) or the Drugs cyclophosphamide (chemo drug and used to treat some vasculitis conditions) and phenacetin (pain drug).
What does BPH increase a man’s risk for?
UTIs (enlarged prostate—> overflow incontinence/ incomplete emptying of bladder—> urine acts as a reservoir for bacteria growth)
*note: BPH is not definitely tied to inc risk for prostate cancer (old age and blacks are at greatest risk for prostate CA)
Substance X is fully reabsorbed at low concentrations, but when the concentrations get high, it begins to spill into the urine. What is substance X?
Glucose. (There is a transport maximum concentration of 200 and rate of 375 in which the transporters are overwhelmed, can’t reabsorb all the excess glucose, and so some stays in renal tubules and is peed out).
What regions (2) of the nephron are particularly susceptible to ischemic damage (as in acute tubular necrosis)?
The PCT and the thick ascending limb of Henle
(These areas have a lot of work to do. For example, the PCT reabsorbs most stuff, so needs a lot of blood to get a lot of oxygen for ATP/ energy to transport stuff across)
What kind of bacteria (I list 3) can cause ammonium magnesium phosphate kidney stones (also known as struvite stones or staghorn calculi?
Proteus mirabilis, staphylococcus saprophyticus, and Klebsiella
(Urease positive organisms)
What is the most common nephritic syndrome in kids? Most common vasculitis in kids?
IgA nephropathy.
Henoch-Schonlein Pupura (which is the same thing as IgA nephropathy + palpable purpura on buttocks and legs. Think of it as the small vessel vasculitis causes problems in the kidney).
