5.02 Approach to Px w/ Renal Disease and Urinary Abnormalities Flashcards

Question

Evaluation of hematuria

Answer 1

If there’s hematuria, check if there’s presence of proteinuria (>500 mg/day) and presence of dysmorphic RBCs or RBC casts. If yes, then proceed ot the R part of this algorithm so can already request for serologic and hematologic evaluation and then sched px for kidney biopsy. If none, check if px has WBC or WBC casts. If there is, then you can request for urine culture to rule out infection or urine eosinophils to rule out interstitial nephritis. If none, can proceed w/ the ff tests: hemoglobin electrophoresis, urine cytology, urinalysis (UA) of family members, and 24 hr urinary calcium/uric acid determination. So Hgb electrophoresis, maybe you are already considering a hematologic d/o causing the hematuria. Urine cytology to rule out malignancy. UA of fam members to check if they have hereditary nephritis or other hereditary GNs. Hyperuricosuria and hypercalciuria can be the risk factors for having microscopic hematuria. If none, can do IVP or renal ultrasound as indicated if there’s a stone or some blood circulation problems, you can do retrograde pyelography or arteriogram. If there’s a cyst, if there’s an indication, you can do cyst aspiration. If none, proceed w/ cystoscopy. If you found out that there is a bladder mass, you can do a biopsy. If none, you can do a kidney (renal) CT scan. If there’s a mass then you can proceed w/ biopsy. If none and you have exhausted all work-ups and didn’t find anything, you can always advise the px to have follow periodic UA. So this will be classified as asymptomatic urinary abnormality.

Answer 2

a. Pyruria - x > 5-10 wbc/hpf (10 if px is pregnant) - Infection, inflammatory, or glomerular dse - WBCs + bacteria = infection - WBC + bacteria + WBC cast = pyelonephritis - Remember not all the time bc of infection that px has pus or pyuria. There are certain conditions when they can also present w/ WBCs so in inflammatory states or even when they have glomer dses b. Casts - Cylindrical structures formed in the DCT and CD and present in the urine in certain disease states - Brought about by the precipitation of Tamm-Horsfall mucoprotein and Albumin - Pronounced in environments favoring protein denaturation and precipitation (low urine flow, concentrated salts, low pH) - Generally, maintained their shape and composition as they pass through the urinary system

Answer 3

Name the crystal and etiology, if possible. 1. Irregularly-shaped - Crystal: Urate - Etiology: Ammonium biurate, uric acid 2. Coffin-shape - Crystal: Triple phosphate - Etiology: Infection 3. Envelope- or rhomboid-shaped - Crystal: Calcium oxalate - Etiology: Most common 4. Hexagonal - Crystal: Amino acid (Cysteine) 5. Fine, needle-shaped - Crystal: Amino acid (Leucine) *Not mentioned anymore: Sulfonamide

Answer 4

a. Considered significant if x > 150 mg/day protein Normal urine protein excretion: x < 150 mg/day Normal albumin excretion: x < 30 mg/day b. Quantifying proteinuria Can be quantified by 24-hr urine collection, urine albumin-creatinine ratio, or urine electrophoresis c. Microalbuminuria - Hallmark of early renal dse - Up to 300 mg albumin/day; dipstick can be negative d. Selective vs. Non-selective - Wrt albumin e. Glomerular vs. Tubular - Tubular protein excretion should NOT exceed 1g/day - Glomerular if more than 3500mg/day such as in nephrotic syndrome

Answer 5

Glomerular origin

Answer 6

UACR - Ratio between two measured substances: urine albumin and urine creatinine - Estimates 24 hr urine albumin excretion - Albuminuria: x > 30 mg/g UACR = marker of CKD

Answer 7

Overflow - Inc plasma conc of free-filtered proteins - Proteinuria: Bence-Jones Glomerular - Abnormality of the glomerular BM - Proteinuria: Albuminuria Tubular - Dec tubular reabs of normal amts of filtered proteins - Proteinuria: Beta-2 or Alpha-1 microglobinuria Secreted - only one among the four that is considered physiologic - Protein renal origin - Proteinuria: Tamm-Horsfall proteinuria

Answer 8

So again we use the urine dipstick and then later on we quantify by requesting for 24 hr urine collection or the 1st morning spot a-to-cr ratio. So if the albumin is around 30-300, we know px has microalbuminuria and these ff cond can bring abt microalbuminuria. But if px has 300-2500, check if px has RBCs or RBC casts on urinalysis. Then these are the conditions, the myeloma-associated kidney dse. And what if px has more than 3500 mg/day of protein spillage or albumin spillage, then px already has nephrotic syndrome. Check for present of RBC or RBC casts on urinalysis. As mentioned a while ago, if there’s RBC casts already, there’s an indication for us to do early kidney biopsy

Answer 9

- Azotemia - reduction in GFR (have an elevated serum creatinine and BUN) - Brought about by AKI and CKD

Answer 10

Consequences of Nephron Injury 1. Nephron loss - leading to: a. dec EPO b. kidney size - Exceptions: DM nephropathy (normal sized in UTZ), amyloidosis, polycystic kidney dse c. inc single nephron glomerular filtration rate - overworked functional nephrons because they take over the diseased nephrons d. dec NH3 production - causing metabolic acidosis * Slide 68: Complications that may arise among px w/ CKD* 2. Abn urine constituents 3. Selective tubule defects - Polyuria (inapp response to ADH) - Hyponatremia (inability to conserve NaCl) - Renal tubular acidosis

Answer 11

Clinical Manifestations of Nephron Injury 1. Hyperkalemia - arrhythmias 2. Acidosis - Kussmaul breathing 3. Stone formation - pain when voiding 4. HypoNa - hypotension, seizure, neurologic NOTE: Not all px w/ kidney damage should be put on salt restriction because some of them are salt-wasting.

Answer 12

Major Nephrology Syndromes: Syndromes of Nephron Injury A. Acute Nephritis (AN) -Usual cause: Transient inflammatory dses of the glomeruli -Prototype: Acute post-strep GN (1 wk hx of sore throat and/or 2-3 wjs hx of skin infection) -Hallmark: Hematuria AN = Nephritic hematuria + azotemia (dec GFR) w/ well-preserved tubule fxn -Clues to dx: Hematuria (blood- or tea-colored urine), dysmorphic RBC (“mickey mouse shaped” from the glomeruli), RBC cast, azotemia, oliguira, edema, HPN

Answer 13

Major Nephrology Syndromes: Syndromes of Nephron Injury B. Nephrotic Syndrome -Usual cause: 1’ or 2’ (e.g. Diabetes, SLE, HBV) - Prototype: Minimal change disease (commonly seen in children, present w/ selective proteinuria mainly albumin) - Hallmark: PROTEINURIA - Clues to dx: - x > 3.5 g proteinuria/day mainly albumin - Hypoalbuminemia - Pitting Edema - Hyperlipidemia

Answer 14

For AKI network: 3 stages (measures serum creatinine and UO) ``` For Rifle Criteria R - risk of renal injury I - injury to the kidney F - failure of kidney fxn L - loss of kidney fxn E - end-stage dse ```

Answer 15

Major Disease Categories causing AKI 1. Prerenal Azotemia - Incidence: 55-60% - Caused by: Acute renal hypoperfusion 2. Intrinsic Renal Azotemia - Incidence: 90% from ATN - Caused by: Acute diseases of renal parenchyma (ATN, etc.) 3. Postrenal Azotemia - Incidence: x < 5% - Caused by: Acute obstruction of the urinary tract

Answer 16

Abdominal compartment syndrome - increased intraabdominal pressure leading to ischemia and organ dysfunction. Under prerenal azotemia etiology

Answer 17

Acute Tubular Necrosis - Tubular injury that can be ischemic (50%), nephrotoxic (35%), or multifactorial (combination of the two) - Note: Profound ischemic injury may result into bilateral cortical necrosis

Answer 18

There is a need to differentiate prerenal azotemia from intrinsic renal failure or the ATN. The way to differentiate them, you have to use the ff indices. *slide* BUN/Pcr ratio - Prerenal Azotemia: x > 20:1 - Oliguric Acute Renal Failure (Intrinsic): x = 10-15:1 Urine Na: Less than 20 = prerenal bc in prerenal, you’re trying to conserve all the fluids, all the Na in the blood in the body to establish or reestablish hemodynamic stability. Remember where Na goes, water follows so less than 20 solute. Urine osmolality is more than 500. Ofc bc you’re trying to put out less vol of urine as much as possible. You will conserve as much fluid as possible to reestablish hemodynamic stability. So putting out concentrated urine. Need to compute for FeNa or fractional excretion of sodium so usually the result is less than 1 for prerenal azotemia for those with intrinsic ATN, renal failure, usually more than 20 Fractional excretion of Sodium = (Una x Pcr x 100)/(Ucr x Pna) Urine/plasma Cr ratio usually more than 40 if prerenal if intrinsic or ATN usually less than 20. Or can simply check urinalysis for presence of hyaline or granular casts, probably px is still on prerenal stage but if you appreciate muddy brown cast, px is on ATN. Why do you need to differentiate? Bc this will have an impact on the management. If px is already on ATN or intrinsic renal failure, you have to be more careful w/ hydrating px, more wary on using some medications.

Answer 19

If the obstruction is bilateral or obstruction is unilateral w/ a dysfxnal or absent contralateral kidney, renal failure manifests. *If unilateral + fxning contralat kidney = plasma crea is normal or only mildly elevated.

Answer 20

Major Nephrology Syndromes: Syndromes of Nephron Injury Chronic renal failure -Azotemia-uremia progressing over more than 3 months or years Clues to dx: - Bilateral small kidneys - Broad casts - Signs of renal osteodystrophy - Half nail signs - nails w/ dark periphery and light center BUT this is not pathognomonic of CKF since it can be found in px w/ nutri deficiencies - Ruger Jersey spine in renal osteodystrophy - alternate dense and rarefied bands on Xray

Answer 21

Stage 1: eGFR >/ 90 *Px has normal GDR but w/ albuminuria!! Stage 2: 60 - 89 Stage 3: 30-59 Stage 4: 15-29 Stage 5/ESRD: x < 15 Table showing the diff stages of CKD. Note that when we say stage 5, it’s also what we now as the end-stage renal dse, the eGFR is less than 15% so when you say eGFR = estimated GFR. So usually px will require dialysis or transplant and then when we check on stage 1, you can see that the GFR is still normal (more than 90) but what’s the catch? Px already has albuminuria so that’s why stage 1. Stage 4 - need to prep px for possible kidney replacement therapy e.g. hemodialysis, peritoneal dialysis, and kidney transplant. How do you prepare? For hemodialysis, ask px to get fistula so usually they undergo surgery to have a fistula. For those transplant, tell them to get a donor already. Note: that stage 3 is further subdivided in 3a and 3b based on the eGFR.

Answer 22

Diabetic Nephropathy Glomerulonephritis Hypertensive nephrosclerosis

Answer 23

So we can eval by again: requesting for US and urinalysis. If on US you will see that the parenchyma of the kidneys are already small, you have a v thin cortex meaning less than 1, you have bland sediments or isosthenuria, most probably px already has CKD. But on US if you saw that px has hydronephrosis, that means there’s an obstruction and there is a need to have this px to undergo urologic evaluation to relieve the obstruction. If there’s normal sized kidney parenchyma, then most prob px has AKI lang. Check UA, if normal urine but w/ oliguria, proceed w/ urine electrolytes to measure the FeNa. You need to request also for urine osmolality. FeNa <1, U osmo > 500 point to prerenal azotemic states; but if more than 1 FeNa and less than 350 U osmo, then px already has ATN. Abn urinalysis, you saw muddy brown cast, ATN na yan. What if there’s bacteria? Then px has pyelonephritis. Presence of WBC, casts, eo then prob intersitial nephritis. What if presence of RBCs lang - then check for blood circulation? Is the renal a. or v. occluded? If yes, you can check/verify that by requesting for angiogram. If there are presence of RBC cast or proteinuria, again you have to do renal biopsy to check for GN and even vasculitis.

Answer 24

Major Nephrology Syndromes: Syndromes of Nephron Injury Tubule Defects - Manifestation depend on portion of tubules affected - May be anatomic or fxnal Clues - Electrolyte d/o - Polyuria - Tubular proteinuria (normal less than 1g/day) - Nocturia - Signs of renal osteodystrophy - Large kidneys (Polycystic renal dse) - Renal transport defects

Answer 25

Major Nephrology Syndromes: Syndromes of Nephron Injury Asymptomatic Urinary Abnormalities - Manifestations: (+) casts, cells, submassive glomerular proteinuria - Dx: BY EXCLUSION!! Manif but on work ups, doesn’t meet any category or any syndrome so this is a dx by exclusion so all other syndrome MUST BE ABSENT to dx this

Answer 26

Obstruction -Luminal Narrowing docu by X-ray, surg, or endoscopy If upper tract - Acute unilateral - no dec in UO bc nagwwork pa urinary tract - Acute bilateral - Anuria/oliguria - Chronic bilateral - hyperkalemia, RTA, or even nephrogenic DI; px who underwent radiation If lower tract - commonly seen in males with BPH - Manif: slow stream, hesitancy, urinary retention, nocturia

Answer 27

UTI - Bacteriuria > 10^5 colonies per mL - Clues to dx: Pyuria, leukocyte casts Location Lower tract (cystitis) -Dysuria, frequency, and urgency, bladder tenderness ``` Upper tract (acute pyelonephritis) -Flank tenderness ```

Answer 28

Nephrolithiasis -Difficulty in passage of urine due to urinary stones -Radio Findings: if w/ obstruction: cortex thinned out, dilated calyceal system, stones in calyces -Tx: surgical removal of stones Types of stones: Calcium Oxalate - most common stone Uric Acid stone - lamellated inner core, dissolved in alkalinized urine Cystine stone - found in urinary bladder and may cause hydronephrosis Staghorn calculi - seen in plain film KUB, fill the collecting systems, radiopaque, branched - most difficult to treat - causes severe hydronephrosis