Nephrology

1
Nephrology
2
Recall the composition of renal calculi in the
setting of chronic UTI

• Struvite (infection) stones
• Magnesium ammonium phosphate
• Urease producing bacteria
• These organisms spit urea and cause persistently
  alkaline urine
• Staghorn shaped stones
• Tx abx eradication and stone removal

3
Recognize the clinical presentation of distal
renal tubular acidosis in an adult pt with
Sjogrens syndrome

• Classic Distal RTA Type I
• Defect H excretion
• Diseases Sjrogens, Stones, Obstruction
• Stones (other RTAs NO stones)
• Serum K low
• Urine pH gt5.5 (other RTAs lt5.5)

4
Recall the diagnostic w/u for a pt with sickle
cell trait who develops hematuria

• REAL BOARD QUESTION!!
• Q. A 19 y/o with sickle cell trait presents with
  microhematuria. BUN/Cr 14/0.8. Urine analysis
  shows RBC gt20/hpf. No casts. No protein. 24 hr
  protein collection is 300mg/d.
• What to do next?
• A. cystoscopy
• B. I.V.P
• C. Renal Bx
• D. Do nothing
• Answer B
• Q. What if the IVP is negative? ?do cystoscopy
• W/U algorithm is following US?IVP?cystoscopy

5
Recognize the clinical presentation of a pt with
psychogenic polydipsia

• Q. A 35 y/o man was found in the bathroom and
  brought to the ER. Glucose90, pOx96 RA. Pt
  has h/o schizophrenia. BP 130/84.
• Serum Na110
• Serum K4.0
• Serum Cl88
• Serum CO218
• BUN/Cr 8 / 0.7
• Serum osmol 230
• Urine Na 10
• Urine osm 40
• The most likely answer is
• A. SIADH
• B. Drug abuse
• C. Addisons dz
• D. Psychogenic polydipsia
• E. Hypothyroidism
• Answer D
• urine sodium in SIADH equals dietary intake.

6
Recognize the clinical presentation and renal bx
findings in a pt with analgesic nephropathy

• Q. 65 y/o with h/o HTN, arrythmias controlled on
  amiodarone, HTN controlled on BB, Osteoarthritis
  contolled with NSAIDS, presents with puffiness of
  face on wakin up. B/L pitting edema. U/A 3
  protein, 15-20 WBCs, RBCs 5. 24 hrs urinary
  protein 4g/day. BUN/Cr 80/5.0. Serum albumin
  2.5
• The most likely dx is
• A. amiodarone induce hypothyroidism
• B. RPGN
• C. NSAID induced Nephrotic syndrome
  Interstitial nepritis
• Answer C
• Tylenol, NSAIDs, Caffeine, Codeine
• CT irregular kidney contour
• Bx membranous nephrophathy
• Thickened capillary loops with sub-epithelial
  deposits

7
Recognize the clinical presentation and renal bx
findings findings in a pt with membranous
glomerulonephritis

• Nephrotic syndrome in 95 of pts
• Microscopic hematuria in 15-30 pts
• DVT
• Subepithelial immune complexes along glomerular
  basement membrane

8
Recognize the clinical presentation of CMV in a
renal transplant pt and recall the most
appropriate management

• Fever and fatigue beginning 1 to 6 months after
  transplantation and accompanied by leukopenia or
  thrombocytopenia
• signs and symptoms of tissue-invasive disease,
  most commonly including hepatitis, pneumonitis,
  and gastrointestinal ulceration
• Rare consequences of CMV infection in renal
  transplant recipients include adrenalitis,
  encephalitis, and, as a late event,
  chorioretinitis
• Tx Intravenous ganciclovir
• American Journal of Kidney Diseases April
  2001 Volume 37 Number 4 p659 to p676

9
Recognize the clinical presentation of a patient
with renal cell carcinoma

• The most common presentations
• The Classic Triad
• hematuria 50-60
• abdominal pain 40
• palpable mass in the flank or abdomen 30-40
• Constitutional sxs
• Left testis varicocele
• Erythrocytosis
• NEJMVolume 335865-875 September 19, Number 12
• Renal-Cell CarcinomaRobert J. Motzer, M.D., Neil
  H. Bander, M.D., and David M. Nanus, M.D.

10
Recognize the clinical presentation of a pt with
Ethylene Glycol intoxication

• Present in antifreeze
• Metabolized by ADH to glyoxalate and oxalic acid
• Oxalate precipitates with calcium and deposited
• Renal failure typically occurs
• Osmolal gap
• Abundant urinary calcium oxalate crystals

11
Recognize the clinical presentation of a pt with
Henoch-Schonlein purpura

• A systemic vasculitis with mesangial and
  extrarenal vascular IgA deposits
• Present with the following
• Joint Pain
• Nephritis
• Purpura on lower extremities
• GI bleeding
• Renal failure usually remits spontaneously

12
Recall the management of a pt with difficult to
control HTN(JNC-7)

• Lifestyle modifications
• Na restriction
• Etoh restriction
• Smoking cessation
• Exercise
• Weight reduction
• DASH diet
• Thiazide diuretic as initial Tx (ALLHAT study)
• BP gt140/90 or gt130/80 in CKD or DM
• Without compelling indications
• Stage I (140-159/90-99)?thiazide diuretic
• Stage II (gt160/gt100)? usually thiazide and ACEI
• With compelling indications? drugs for specific
  indication
• Not at BP goal? optimize dosages or add
  additional agent
• Compelling indications
• CHF diurectic, BB, ACEI, ARB, AldoAntag
• Post MI BB, ACEI, AldoAntag
• High CAD risk Diuretic, BB, ACEI, CCB (NKF)
• CKD ACEI, ARB (NKF/ALLHAT)

13
Recognize the clinical presentation of a pt with
possible atherosclerotic dz

• Abrupt onset of severe HTN
• Resistant to effective medical tx
• Target organ damage
• Unprovoked hypokalemia
• ACEI inhibitor induced renal dysfunction

14
Recognize the clinical presentation of a pt with
IgA nephropathy

• Synpharyngitic hematuria
• Hematuria that is provoked or exacerbated by
  pharyngitis
• Development of hematuria and nephritic urine
  within one day or so of an upper respiratory
  infection

15
Recognize the clinical presentation and urine
sediment findings of a patient with
post-infectious GN

• Dark or smoky colored urine and edema, often with
  HTN and sometimes oliguria.
• Follows pharyngitis or impetigo 1-3 weeks later
• Asymptomatic hematuria and non nephrotic range
  proteinuria
• protein, blood, RBCs and WBCs, dysmorphic red
  cells, acanthocytes, cellular (ie, RBC, WBC)
  casts, granular casts, and oval fat bodies
• Anti ASO, Anti DNase B
• Hypocomplementemia

16
Recognize the clinical presentation of a pt with
indinavir-induced nephropathy

• Indinavir excreted in kidneys
• Crystals form in urine
• Crystals may precipitate in renal tissue and
  cause ARF
• Symptoms of dysuria, back/flank pain, colic since
  indinavir kidney stones associated with urinary
  tract obx and postrenal azotemia
• Hematuria and crystalluria provide clues

17
Recall the clinical presentation and initial
diagnostic w/u for a pt with primary aldosteronism

• Headache, HTN, Hypokalemia
• BP resistant to Tx
• Initial Screening
• 1. Ratio of plasma Aldosterone Renin (201)
• Done in am, upright posture dependent
• 2. High sodium diet- 2-3 grams of salt with
  meals for 3 days with a high urinary aldosterone
  excretion
• 3. High plasma aldosterone level after NSS
  infusion
• 4. Sampling of adrenal venous blood with
  corticotropin stimulation-most reliable method
• CT after biochemical assays

18
Recall how to use the delta anion gap and delta
serum bicarbonate to evaluate a patient with
mixed metabolic acidosis

• For every increase in AG, there should be a 11
  decrease in HCO3- level
• This is because HCO3- is the only (normal)
  homeostatic buffer in the blood
• If the change in HCO3- gt change in AG (from
  normal), then a primary acidosis is present
• If the change in HCO3- lt change in AG (from
  normal), then a primary alkalosis is present
• In other words, if expected HCO3- is more than
  measured HCO3-, then excess HCO3- was present
  before acidosis occurred
• Likewise, if expected HCO3- is less than the
  measured HCO3-, then the HCO3- level when the
  anion gap acidosis began was low (i.e. a
  non-anion gap acidemia was present)
• Delta/Delta ?AG/?HCO3
• lt1 acidosis
• gt1 alkalosis

19
Recognize the clinical presentation and
urinalysis results for a pt with rhabdomyolysis

• Precipitated by
• Muscle trauma
• Strenuous exercise
• Influenza
• Potassium or phosphorus depletion, drug overdose
  or etoh abuse
• Cocaine
• HMG-CoA inhibitors
• ARF due to Rhabdo assoc with high serum levels of
  K, Phos, CK, Uric acid

20
Recognize the clinical presentation of a pt with
diabetic nephropathy and recall the most
appropriate treatment

• Microalbuminuria
• Creatinine clearance declines
• Hypertension and proteinuria
• Tx includes
• Lifestyle modifications
• DM control
• HTN control
• Lipid control
• Protein and phosphorus restriction
• Smoking cessation- smoking assoc with accelerated
  renal decline
• ACEI or ARB initiation with target BP 130/80
• NEJM Nephropathy in Patients with Type 2
  DiabetesGiuseppe Remuzzi, M.D., Arrigo
  Schieppati, M.D., and Piero Ruggenenti, M.D.

21
Recognize that hypomagnesemia as a cause of
refractory hypocalcemia

• Hypomagnesemia is known to suppress parathyroid
  hormone release and inhibit the effect of the
  hormone on its receptor, hypocalcemia often
  accompanies severe hypomagnesemia

22
Recognize the distinguishing characteristics of
essential mixed cyroglobulinemia as a cause of
the nephrotic syndrome

• Renal disease may occur secondary to thrombosis
  (type I cryoglobulinemia) or immune complex
  deposition (types II and III)
• membranoproliferative glomerulonephritis is
  almost always the lesion in mixed
  cryoglobulinemia
• Clinically, isolated proteinuria and hematuria
  are more common than nephrotic syndrome,
  nephritic syndrome, or acute renal failure
• Renal involvement is one of the most serious
  complications of cryoglobulinemia and typically
  manifests early in the course of the disease

23
Recall the appropriate therapy for preventing ARF
in pts with crush injuries

• Volume repletion
• Administration of mannitol bicarb
• Bicarb to alkalinize the urine
• Studies lacking showing efficacy after onset of
  renal injury
• Administration of lasix early in the course of
  ARF has been suggested in pts with oliguria
• Dialysis may be necessary if hyperkalemia present

24
Recognize the clinical presentation of a pt with
cancer associated membranous nephropathy and the
nephrotic syndrome

• particularly cancer of the lung, breast, GI tract
  and kidney
• Generally the renal function improves with cure
  of the cancerit is a paraneoplastic process
• Membranous nephropathy is the most commonly seen
  glomerular lesion is cancer pts with nephrotic
  syndrome

25
Recall the role of cystoscopy in the evaluation
of a patient with hematuria whose clinical
features suggest a nonglomerular source

• Usually due to bleeding in urinary tract
• If blood is present evenly throughout voiding
  ("total hematuria") suggests source is bladder or
  above, because blood has had opportunity to mix
  with urine otherwise, probably of urethral or
  prostatic origin
• Causes
• Calculi
• Neoplasm
• TB
• Trauma
• Prostatitis
• Primary renal causes (rare) focal
  glomerulonephritis (usually has RBC casts),
  analgesic nephropathy, sickle cell anemia
  (usually sl. proteinuria, papillary necrosis, and
  azotemia)
• Approach
• IVP and renal u/s
• If no lesion seen, cystoscopy and maybe
  retrograde pyelography

26
Recognize the important risk factors for CV dz in
a pt with longstanding HTN

• Smoking
• Dyslipidemia
• DM
• Age older than 60 yrs
• Sex ( men and postmenopausal women)
• Family h/o CV dz
• Women lt age 65 yrs
• Men lt age 55 yrs

27
Recall the beneficial effects of ACEI in
preventing progression of renal dz in a pt with
hypertensive nephrosclerosis

• Renoprotective effect of ACEI in African-American
  pts with proteinuria and renal insufficiency

28
Recall the clinical presentation of a pt with
Bartters syndrome

• Abnormal chloride transporters in the ascending
  loop of Henle
• Usually dxd in childhood and early teens
• Growth and mental retardation
• Hypokalemia, metabolic alkalosis
• Polyuria, polydipsia, decreased concentrating
  ability of kidney
• Pts are normotensive

29
Lab findings in pt with mixed acid base
disturbance

• Expected PCO2 for any metabolic
  (alkalosis/acidosis) can be calculated as
  follows
• Metabolic acidosis PCO2 falls 1.2 mm Hg for
  every 1 mEq/L fall in HCO3.
• Another formula
• PCO2 1.5 X (observed HCO3) 82 A quick rule
  of thumb The PCO2 should approximate the last
  two digits of pH. For example, pH 7.25, PCO2
  should be close to 25 mm Hg.
• Metabolic alkalosis PCO2 rises 0.7 mm Hg for
  every 1 mEq/L rise in HCO3.
• Inappropriate metabolic compensation for
  respiratory disorders are diagnosed by comparing
  the observed HCO3 with the expected (calculated)
  changes in HCO3 for that observed change in PCO2.
  
• When the observed HCO3 is higher than the
  expected HCO3, a primary metabolic alkalosis is
  complicating the respiratory disturbance.
  Conversely, when the observed HCO3 is lower than
  the expected HCO3, a primary metabolic acidosis
  is complicating the respiratory disturbance.
• Expected HCO3 for any respiratory
  (alkalosis/acidosis) can be calculated as
  follows
• Respiratory alkalosis Acute 2 mEq/L drop in HCO3
  for every drop of 10 mm Hg PCO2.
• Chronic 4 mEq/L drop in HCO3 for every drop of
  10 mm Hg PCO2.
• Respiratory acidosis
• Acute 1 mEq/L increase in HCO3 for every
  increase of 10 mm Hg PCO2.
• Chronic 3.5 mEq/L increase in HCO3 for every
  increase of 10 mm Hg PCO2.
• Mixed metabolic acidosis and metabolic alkalosis
  are diagnosed when the change in the anion gap
  (AG) does not equal the change in HCO3. Because
  the AG is an indirect measure of the acid added
  to the body, the HCO3 should fall by an amount
  paralleling the rise in AG. When the HCO3 is
  greater than the rise of the AG, a primary
  metabolic alkalosis is complicating the metabolic
  acidosis. Conversely, when the HCO3 is less than
  the rise of the AG, a non-AG metabolic acidosis
  should be assumed to be complicating an AG
  acidosis.

30
Recognize the thromboembolic complications of
nephrotic syndrome

• Hypercoagulability is a compication of the
  nephrotic syndrome
• Decrease plasma levels of protein S, protein C,
  and antithrombin III.
• DVT more often than arterial thrombosis
• Thrombosis occur more readily with serum albumin
  lt2.0

31
Recognize the clinical presentation of a pt with
acute interstitial nephritis

• Fever, rash, and eosinophilia
• Sterile pyuria and microscopic hematuria
• Non-nephrotic range proteinuria
• Eosinophiluria differentiates interstitial
  nephritis from ATN, nephrotoxicity and
  pyelonephritis
• Infections and immunologic conditions predispose
• PCN, NSAID, quinolones, diuretics, pepcid,
  dilantin, phenobarb, allopurinol, cephalosporins,
  interferon-a

32
Recognize the clinical presentation of
Goodpastures syndrome

• pulmonary-renal syndrome
• Hemoptysis
• Pulmonary infiltrates
• Hematuria with erythrocyte casts
• Dx confirmed by serum anti-glomerular basement
  membrane antibodies
• Linear immunofluorescent pattern of ab and
  complement deposition on basement membrane

33
Recall how to identify diarrhea as a cause of
metabolic acidosis

• GI HCO3 loss
• Diarrhea
• Pancreatic, biliary, or intestinal fistulas
• Ureterosigmoidostomy
• Cholestyramine

34
Recognize iron deficiency as a reason for failure
of erythropoietin to correct anemia in a pt with
CKD

• Iron used as a substrate with erythropoitin for
  RBC production

35
Recognize the clinical presentation of a pt with
benign orthostatic proteinuria

• Benign positional or orthostatic proteinuria is
  easily dxd with split daytime (standing) and
  nightime (supine) urine collections.
• Generally lt 1g/d
• Uncommon over the age of 30
• Good outcomes in benign positional proteinuria

36
Recall the appropriate treatment of a pt with
hypervolemic hyponatremia

• Treatment of underlying condition
• Cirrhosis
• Nephrosis
• Cardosis
• Salt and water restriction
• May benefit from loop diuretic

37
Recognize surreptitous vomiting as a cause of
hypokalemia

• Unexplained metabolic alkalosis and hypokalemia
  (including exclusion of primary mineralocorticoid
  excess) is usually due to one of three disorders
  
• surreptitious, self-induced vomiting (as with
  anorexia nervosa or bulimia)
• diuretic abuse one of the causes of
  mineralocorticoid excess and
• Gitelman's or Bartter's syndrome in patients who
  are not hypertensive
• Urinary chloride excretion is normally very low
  in patients with vomiting and metabolic alkalosis

38
Recognize the clinical presentation of a pt with
hemolytic-uremic syndrome

• Microangiopathic hemolytic anemia
• Thrombocytopenia
• Acute renal failure
• recent history of diarrhea (possibly bloody)

39
Recognize atheroembolic renal dz as a cause of
renal failure

• Rarely occur spontaneously
• Atheroembolic dz occurs in pts with
  atherosclerosis, especially after angio,
  angioplasty, vascular surgery, IABP,
  anticoagultion, or throbolysis
• Result from cholesterol crystals or debris from
  atheromatous plaques
• Other organs systems effected
• Cerebral ischemia
• Ocular abnormalities
• Intestinal ischemia
• Refractile plaques in retinal arteries-Hollenhorst
  plaques
• Livedo reticularis
• Petechial lesions
• Cyanosis of lower extremity digits
• Eosinophilia and hypocomplementemia
• Bx typical concave clefts in small vessels
• Prognosis of recovery of renal function and pt
  survival is poor

40
Recall how to use the delta anion gap and delta
serum bicarb to evaluate a pt with mixed
metabolic acidosis

• Example
• Q. Na 135 K 5.7 CL 80 HCO3 24 Bun/Cr 110/11
• pH 7.4 pCO237 HCO3 22 this pt most likeley has
• Normal Acid Base
• Metabolic Acidosis with Metabolic Alkalosis
• Metabolic alkalosis with respiratory alkalosis
• Answer A
• 135- (8024) 31
• Change in gap 31-1219
• So HCO3 should really have been 24-195. But it
  is 24. So the additional 19 is from metabolic
  alkalosis.

41
Rocognize the presentation of distal RTA in an
adult pt with Sjogrens syndrome

• Classic Distal RTA Type I
• Defect H excretion
• Dzs Sjorgrens, Stones, Obstruction
• Stones (other RTAs, no stones)
• Serum K low
• U pH gt5.5 (other RTAs lt 5.5)

42
Determine the cause of metabolic alkalosis in a
pt with hypokalemia

• Low urinary Chloride (lt20 meq/L) Cl responsive
• Diuretics (remote)
• Vomiting/NGT
• Status post chronic hypercarbia

• High Urinary chloride (gt20 meq/L) Cl unresponsive
• Diuretics (recent)
• HTN
• Primary Hyperaldo
• Cushings dz
• Ectopic ACTH
• Exogenous mineralcorticoid
• Liddles syndrome
• Low BP
• Bartters syndrome
• Gitelmans syndrome
• Severe potassium depletion

43
Recall the indications for parathyroidectomy in
asymptomatic hypercalcemia

• If PTH gt 1000 ? parathyroidectomy
• 1991 NIH Consensus Conference
• Markedly elevated serum calcium concentration
  (gt11.5 mg/dL)
• Previous episode of life-threatening
  hypercalcemia
• Reduced renal function (creatinine clearance
  CrCl reduced by 30 compared with age-matched
  control subjects)
• Radiologic evidence of kidney stones or
  nephrocalcinosis
• A 24-hour urine calcium level greater than 400 mg
  
• Reduction in bone density greater than 2 standard
  deviations for age-, gender-, and race-matched
  control subjects
• Medical surveillance not suitable or desirable

44
Recall how to calculate the anion gap in a pt
with hypoalbuminemia

• Anion gap falls by 2.5 meq/L for every 1g/dl
  reduction if plasma albumin

45
Recall the criteria for establishing the
diagnosis of autosomal dominant polycistic kidney
dz

• In a pt with PKD1
• In patients younger than 30 years of age, at
  least two cysts (on one or both kidneys) to be
  present.
• In patients aged 30 to 59, at least two cysts in
  each kidney.
• In patients over age 60, four or more cysts in
  each kidney.