Category Archives: Nephrology

VA Ambulatory Report 2.21.18 – Sarcoid Diagnosis and Hematuria

We had two great case discussions today.

First Jeff presented an image of incidentally discovered pulmonary nodules and hilar lymphadenopathy.  The patient was diagnosed with sarcoid based on these imaging results alone.

Learning points:

  • How to diagnosis sarcoid:
    • If a patient is asymptomatic with characteristic radiographic findings – this is sufficient to make the diagnosis
    • For symptomatic patients, biopsy confirming noncaseating granulomas is required
  • For a new diagnosis of sarcoid monitor for complications and extrapulmonary involvement: EKG, eye symptoms, vitamin d levels, UA
  • In an asymptomatic patient with low grade radiologic changes, the management is observation only


Second, Akshai presented a patient seen in clinic the day prior with gross hematuria.

Learning points:

  • Gross hematuria should strongly increase your suspicion of malignancy. The incidence of malignancy in microscopic hematuria vs. gross hematuria  is ~2% vs. 20%.
  • Smokers are 4-7 times more likely to develop bladder cancer than non-smokers
  • CT Urography is the test of choice to evaluate for malignancy and nephrolithiasis.  CTU provides both functional and anatomic information about the kidney and ureter.  The pre-contrast phase evaluates for nephrolithiasis and hydronephrosis.  The post contrast phase evaluates renal and urothelial malignancies and can assess kidney function in the setting of obstruction.


Evernote link:


Moffitt Pearls 12.15.17 + Intern Pearls

Hey Moffitt!

Sorry for delay…better late than never! Thank you to Jill and Emily for presenting a fascinating case of middle aged man with hx of chronic wounds and HCV s/p presenting with foamy urine found to have nephrotic Syndrome, possibly membranous nephropathy based on tempo, demographics and history. Unfortunately patient left the hospital AMA prior to renal biopsy.

HH’s CRANKLES Nephrotic Syndrome Mneumonic: Blast from the past!!!

C –Cardiac/pericarditis

R – renal vein thrombosis

A – Amylodosis and paraproteinemias

N – MCG, FSGS, Membranous (unusual, but possible to have MPGN or IgA Nephropathy)

K – Kimmelesteil and Wilson nodular intercapillary lesions (Diabetes – most common cause world wide)

L – Lupus

E – Eclampsia

S – Secondary syphilis

Nephrotic Syndrome

Definition: > 3.5 g urine protein/day, hypoalbuminemia (< 3 g/dL), peripheral edema. Associated HLD and thrombosis can be present. Hypertension is more common in nephrotic syndromes. 

Differential Diagnosis – see above 

Other associated findings: acute kidney injury (not always), thromboembolism (renal vein thrombosis is found disproportionately in patients with membranous nephropathy), infection (due to urinary loss of immunoglobulins), proximal tubular dysfunction

Biopsy is often necessary to reveal the definitive diagnosis. (note this is in contrast to nephritic syndrome, which can be diagnosed with examination of the urine sediment and blood work: serologies). Interestingly, Richards, et al* found that in 28 patients with nephrotic range proteinuria, histologic information obtained via biopsy altered management in 24/28 cases (86%!!!)

Treatment: Diuretics (treat edema), Ace-inhibitor (proteinuria), statin (hyperlipidemia), anticoagulation (hypercoagulability)

Membranous Nephropathy 


In non-diabetics this accounts for up to 1/3 of cases of Nephrotic Syndrome. Especially common among white men.

Breakdown in primary vs secondary causes:

MN is most often primary (idiopathic), associated with the presence of anti-PLA2R antibodies (can be measured in serum); although, it has been associated with a variety of conditions, including hepatitis B antigenemia; autoimmune diseases (eg, lupus); malignancy; and the use of certain drugs such as gold and nonsteroidal antiinflammatory drugs (NSAIDs). MN may also be seen in conjunction with other glomerular diseases such as diabetic nephropathy and crescentic glomerulonephritis.

First pass work-up (per up-to-date)

  • CMP + Albumin
  • CBC
  • UA with examination of the sediment
  • Protein/Creatinine ratio or 24 urine for protein
  • Tests for hepatitis B & C  & HIV
  • Serum C3 and C4 complement levels
  • In patients older than 50 years – serum free light chains (SFLCs) and serum protein electrophoresis (SPEP) with immunofixation
  • Anti-PLA2R antibody (by enzy


  • Based of risk if progression given low risk disease often spontaneously resolves without therapy (see link for more info).
  • First-line immunosuppressive therapy consists of cytotoxic drugs (cyclophosphamide) plus glucocorticoids or a calcineurin inhibitor with low-dose or no glucocorticoid.

Intern Report Pearls

Virchow’s Triad – RF for clotting

  1. Hypercoagulable
  2. Stasis
  3. Endothelial damage

Compartment Syndrome

  1. Pain
  2. Pallor
  3. Pulseless
  4. Poikelothermia
  5. Paralysis
  6. Paresthesias

Phlegmasia cerulea dolens (painful blue edema) is an uncommon severe form of DVT which results from extensive occlusion (blockage by a thrombus) of the major and the collateral veins of an extremity.

Evaluation of Isolated Elevated PTT

  • Contamination
  • Deficiency
  • Inhibitor – factor 8 is the most common inhibitor

When concerned about an inhibitor order a mixing study – does not correct with mixing study.

Clotting & Bleeding – Causes 

  • APS
  • DIC
  • HIT
  • Liver Disease

Management of Bleeding with Inhibitor 

Give factor back or bypass cascade – PCC or FEIBA, Novo 7

Steroids – Prednisone 1 mg/kg per day

Rituximab or Cyclophosphamide



Acquired Inhibitor – Causes  • Underlying Cancer

  • Exogenous exposures
  • Autoimmunity
  • Medication related
  • Pregnancy
  • Idiopathic – ~50% cases unknown cause

Moffitt Renal Report Pearls– 11.17.17

Thank you to HH and Katie for co-presenting a case of a young woman with T1DM, CKD presenting with a severe non-anion gap metabolic acidosis with a pH of 7 and a Bicarb of 6! Overall, it was felt that her initial presentation was 2/2 to a mix of GI losses given her profound diarrhea and renal losses of bicarb in early renal dysfunction.

Key Pearls:

  1. When calculating the serum anion gap, there’s no need to correct serum sodium for hyperglycemia. The osmotic pull of water would dilute all of the electrolytes in an equal manner, so the sodium, potassium, and chloride are all relatively dilute, and the anion gap calculation would not change.
  2. When trying to determine where a patient is losing bicarbonate – you can calculate a urine anion gap UAG – see more below.
  3. In a patient with normally functioning kidneys, they will secrete ketones in their urine. In patients with DKA, this can eventually result in a non-anion gap acidosis.
  1. Remember risk factors for central pontine demyelination with rapid correction > 10 in 24 hours include: very low sodium levels < 110 (in most cases), premenopausal females and severe malnutrition.

Urine Anion Gap (UAG)

Na +  K  –  Cl = Ur Anion Gap (this is calculating unmeasured anions NH4+ primarily)


  • Assumes that the patient is volume replete (Una > 20) and is without an anion gap acidosis
  • If UAG + in setting of non-gap metabolic acidosis this suggests the kidneys are FAILING to excrete ammonia à renal tubular acidosis
    • DDx: RTAs (see below)
  • If UAG zero or negative, suggests bicarbonate losses from GI tract (this means the kidneys are appropriately getting rid of NH4+ to compensate for acidosis).
    • DDx: GI losses (diarrhea or fistulas), early renal failure& ingestions
  • These labs must be interpreted in the context of patient’s presentation and there are not strict cut-offs.
  • Depending on the severity of the metabolic acidosis, if you have normal kidneys, the urine anion gap should be even more negative (kidney is responding appropriately to excrete NH4+).
  • If you have severe metabolic acidosis, and the urine anion gap is zero or only slightly negative, this suggests a mixed picture – in that there are GI losses, but the kidney’s are not responding as robustly as they should to get rid of NH4+. With excretion of NH4+ the CL- amount increases and this should drive the equation above more and more negative.

Non-Gap Acidosis Ddx

  • GI losses of HCO3- Diarrhea, fistulas/drainage
    • Proximal (Type II): decreased reabsorption & then loss of HCO3-
    • Distal (Type I): defect in H+ excretion (hence profound acidosis)
    • Hypoaldo (Type IV): acidosis 2/2 to inability to excrete acid
  • Early renal failure – impaired generation of NH4+ (this is the KEY to understanding the physiology per above)!
  • Ingestions – acetazolamine, sevelamer, toluene
  • Dilution – rapid infusion of bicarb free IVFs
  • Post-hypocapnia – Rapid correction of respiratory alkalosis -> renal wasting og HCO3 needs to be regenerated
  • RTAs
Location Type Acidosis UAG U pH FeHco3 Serum K
Proximal II Moderate +/- <5.3 > 15% LOW
Distal I Severe + > 5.3 < 3% Variable
Hypoaldo IV Mild + > 5.3 < 3% HIGH




Moffitt Pearls 10/30/17 – Palpable Purpura + AKI

Thank you, Lily for presenting a case this morning of a middle-aged woman from Mexico being treated for a metastatic GI malignancy p/w flank pain, AKI and palpable purpura found to have obstructive nephropathy and candiduria .

Key Pearls:

  1. Classic approach to AKI: pre-, intrinsic-, post-renal hold-up even when the patient becomes more complicated. Always remember to consider carefully a patient’s volume status and run the med list.
  2. The DDx for purpura can be broken down first by whether or not the lesions are palpable. If NOT palpable, we call these petechiae or ecchymoses based on the size (<3mm = petechiae). This should prompt consideration of the coagulation cascade, platelets, uremia. If palpable, this suggests inflammation and a possible vasculitis. See an approach to palpable purpura below.
  3. Yeast in urine is usually a colonizer and not a pathogen. However, treatment for funguria is indicated in patients with renal transplant and immunosuppression. See link for more info
Candiduria: A Review of Clinical Significance and Management – Zakeya Abdulbaqi Bukhary

Selected Highlights:

  • Treatment of Candida can be guided by in vitro susceptibility testing (although all labs do not send these).
  • Fluconazole gains high concentrations of active drug in the urine, is better tolerated and is less likely to be associated with the emergence of resistance during therapy.
  • The greatest concern for fluconazole resis­tance is related to C. glabrata and C. krusei isolates which require maximal doses of amphotericin B.
  • As HH mentioned – Echi­nocandin anti fungal agents (caspofungin, micafungin, and anidulafungin) can be used although low sub-therapeutic levels are achieved in the urine because the drug has poor glomerular filtration with subsequent diminished tubular secretion. 

More Info at:


Causes of Non-Palpable Purpura based on size of lesion

  • Remember these lesions are macular and are typically NOT inflammatory
  • Petechiae (small lesions < 3 mm)
    • Abnormal palatele function
    • Increased intravascular pressures
    • Thrombocytopenia
      • Idiopathic
      • Drug-induced
      • Thrombotic
    • DIC and infection
  • Ecchymoses (larger lesions > 5 mm)
    • Coagulation defects
    • DIC and infection (purpura fulminas)
    • External trauma
    • Hypergammaglobulinemic purpura

See the following link for more information in a case based ppt from the American Academy of Dermatology Titled “Petechiae, Purpura and Vasculitis.”

Break down Vasculitis based on vessel size



VA Ambulatory Report 10.4.17 – Nephrotic Syndrome

Thanks to Akshai for presenting an interesting case of a 41 yo F with subacute bilateral leg swelling found to have nephrotic syndrome in the process of being evaluated for the underlying cause.



  • Proteinuria can be broken into 4 causes: Overflow, glomerular, tubular, post-renal
  • When concerned about a glomerular process use your clinical findings and UA to help you determine if the picture is more consistent with nephritic vs. nephrotic
  • Nephritic Syndrome is often diagnosed with lab tests whereas nephrotic syndrome usually needs a biopsy to confirm the underlying cause
  • Treatment of nephrotic syndrome: ACEi/ARB for proteinuria, loop diuretic and salt restriction for edema, statin if hyperlipidemia does not resolve, warfarin if thrombosis.


What is the usefulness of BNP for lower extremity edema?

  • Breathing Not Properly Study: In a patient presenting with dyspnea a BNP cut off of > 100 can be helpful in determining heart failure over pulmonary cause of dyspnea
  • The ACC/AHA 2017 Focused Update gives a Class I recommendation for measurement of BNP in patients presenting with dyspnea, to support a diagnosis or exclusion of HF.
  • No studies have looked at BNP in a patient presenting with lower extremity edema as a predictor for heart failure
  • Can be elevated for a variety of reasons:  renal failure, cirrhosis, sepsis, anemia, stroke, OSA, PE and more.


Causes of Proteinuria (Forgive my powerpoint nephron drawing!)

Screen Shot 2017-10-06 at 10.10.50 AM.png

Nephritic vs. Nephrotic?

Disease of the glomerulus can be nephrotic or nephritic.  Use your clinical findings and UA to help you differentiate.

  Clinical Findings UA and urine sediment Findings Histology Findings
Mild Nephritic Asymptomatic microscopic hematuria and proteinuria

Occassionally gross hematuria

RBCs, dysmorphic RBCs, RBC casts

Mild proteinuria

Inflammatory lesions in less than one half of glomeruli
Severe Nephritic Edema


Renal Insufficiency

RBCs, dysmorphic RBCs, RBC casts

Heavy Proteinuria (>1.5g/day)

Diffuse glomerular disease
Severe Nephrotic Hyperlipidemia


Thrombotic disease

Heavy proteinuria (oftenr >3.5g/day)

Few casts or cells

Varies based on underlying cause


Nephrotic Range Proteinuria work-up for the PCP:

  • Send ANA, A1c, HIV, RPR, and Hepatitis serologies.
  • Refer to renal for likely renal biopsy.
  • Renal biopsy is often needed in adults whereas children are often treated with empiric steroids for presumed minimal change disease.


Treatment of Nephrotic Syndrome

  • Proteinuria
    • The degree of proteinuria is a predictor of renal failure. Treatment can reduce progression.
    • ACEi/ARBs – BP effects are immediate but proteinuria effects can take days-weeks
  • Volume Overload:
    • Due to sodium retention (not oncotic pressure from protein loss)
    • Diuretics; Slow diuresis to prevent hypovolemia, start with loop diuretics but may also need thiazide diuretics
  • Hyperlipidemia
    • Often reverse when underlying cause is treated and reversed
    • Most patients will need statin
    • Dietary modification does not help
  • Hypercoagulability
    • More common in membranous nephropathy
    • If thrombosis, treat with warfarin
    • Unclear if prophylactic anticoagulation benefit outweighs risks, practice varies amongst nephrologists
  • Treat underlying cause if identified


Hey everyone! Thanks to Luis for presenting a case of a middle-aged man with infectious symptoms and NSAID use who developed a complex renal picture of AKI, proteinuria/hematuria, white cell casts, and confusing hepatitis serologies. We touched on nephrotic syndrome and AIN.


Top Pearls:

  1. WBC casts usually indicate interstitial nephritis but can also represent glomerulonephritis.
  2. Only 3% of AIN patients have WBC casts in their urine. Eek!
  3. Only 10% of AIN patients have the classic triad of rash, fever, and eosinophilia.


For those who want more info:

WBC casts are insensitive, and also not totally specific, for AIN. Only 3% of AIN patients have WBC casts in their urine, and WBC casts can rarely represent glomerulonephritis even though we usually think of GN associated with RBC casts.

We have covered nephrotic syndrome a fair number of times in report this year. Check it out:

Also here is a prior discussion of causes of interstitial nephritis, also touching on low anion gap which came up today:

Additionally, the classic AIN triad of clinical manifestations is rash, fever, and eosinophilia. However, the incidence of each of these findings, as well as the full triad, is not very high:

Rash- 15%

Fever- 27%

Eosinophilia- 23%

Triad- 10%

Lastly, we talked about NSAID-induced renal dysfunction, which is reviewed here:

*Pearl: NSAID-induced AIN does NOT usually present with the classic manifestations noted above.




Have a great day everyone!


MOFFITT RENAL REPORT PEARLS 2/24/17: Myeloma Kidney!

Thanks to Dr. Gluck for presenting an interesting case of AKI on CKD, as well as megaloblastic anemia, who turned out to have newly diagnosed multiple myeloma! Pearls below:


Top Pearls:

  1. Renal biopsy is usually indicated to prove the association between myeloma and renal injury.
  2. Treatment of myeloma kidney is chemotherapy, steroids, hydration, and possibly plasmapheresis.


For those who want more info:

Multiple myeloma is a popular topic at Moffitt! Here are some previous blog posts:

Since this was renal report, let’s review myeloma kidney!

Kidney disease is one of the most common complications of MM due to a wide range of mechanisms and usually occurring in patients with large tumor burden.

In MM patients, AKI is most commonly due to light chain cast nephropathy, hypercalcemia, and nephrotoxic agents (e.g. NSAIDs). MM is also a cause of nephrotic syndrome!

Most patients with MM who have kidney disease undergo renal biopsy to confirm the association between monoclonal protein and kidney disease (some exceptions).

Treatment for AKI due to MM light chain cast nephropathy is chemotherapy and steroids, in addition to hydration, correction of hypercalcemia, and discontinuation of nephrotoxic agents (NSAIDs, ACEs, ARBs).

There is some data for plasmapheresis to remove light chains, which has shown a possible reduction in dialysis dependency among survivors, but this is controversial.

Dialysis indications are the same as in non-myeloma patients.




Have a great day everyone!