Focal segmental glomerulosclerosis - Revision history

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Ostermayer: Created page with "Focal segmental glomerulosclerosis (FSGS) is a pattern of '''glomerular scarring''' in which sclerosis affects '''segments''' (not the entirety) of '''some''' (not all) glomeruli.Focal Segmental Glomerulosclerosis. ''StatPearls''. NCBI. 2024. It is the '''most common cause of primary (idiopathic) nephrotic syndrome in adults''' in the United States and the '''leading glomerular cause of end-stage kidney disease (ESKD)'''.Ros..."

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Created page with "Focal segmental glomerulosclerosis (FSGS) is a pattern of '''glomerular scarring''' in which sclerosis affects '''segments''' (not the entirety) of '''some''' (not all) glomeruli.<ref name="StatPearls">Focal Segmental Glomerulosclerosis. ''StatPearls''. NCBI. 2024.</ref> It is the '''most common cause of primary (idiopathic) nephrotic syndrome in adults''' in the United States and the '''leading glomerular cause of end-stage kidney disease (ESKD)'''.<ref name="CJASN">Ros..."

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Focal segmental glomerulosclerosis (FSGS) is a pattern of '''glomerular scarring''' in which sclerosis affects '''segments''' (not the entirety) of '''some''' (not all) glomeruli.<ref name="StatPearls">Focal Segmental Glomerulosclerosis. ''StatPearls''. NCBI. 2024.</ref> It is the '''most common cause of primary (idiopathic) nephrotic syndrome in adults''' in the United States and the '''leading glomerular cause of end-stage kidney disease (ESKD)'''.<ref name="CJASN">Rosenberg AZ, Kopp JB. Focal Segmental Glomerulosclerosis. ''Clin J Am Soc Nephrol''. 2017;12(3):502-517.</ref> FSGS disproportionately affects '''African Americans''' (driven by APOL1 risk alleles). The emergency physician encounters FSGS patients presenting with '''nephrotic syndrome''' (massive edema, proteinuria, hypoalbuminemia) and its '''life-threatening complications''': '''thromboembolism''', '''spontaneous bacterial peritonitis''', '''hypovolemic crisis''', '''acute kidney injury''', and '''severe hypertension'''.

==Background==
*'''Diagnosis is histopathologic''' — requires renal biopsy; cannot be diagnosed by clinical features or labs alone<ref name="StatPearls"/>
*FSGS accounts for ~35% of nephrotic syndrome in adults (higher in Black patients) and 7-20% in children
*Incidence is increasing worldwide over the past three decades<ref name="MSD">Focal Segmental Glomerulosclerosis. ''MSD Manual Professional Edition''. 2025.</ref>

===Classification===
{| class="wikitable"
|-
! Type !! Mechanism !! Key features
|-
| '''Primary (idiopathic)''' || Presumed circulating permeability factor injuring podocytes || Nephrotic-range proteinuria; responds to immunosuppression; '''recurs in up to 40% of kidney transplants'''
|-
| '''Secondary''' || Adaptive (hyperfiltration) or toxic podocyte injury || Obesity, HIV (HIVAN), heroin, sickle cell, reflux nephropathy, single kidney, anabolic steroids; usually subnephrotic proteinuria
|-
| '''Genetic''' || Mutations in podocyte structural proteins (NPHS1, NPHS2, INF2, TRPC6, others) || Steroid-resistant; does NOT recur after transplant; family history
|-
| '''APOL1-associated''' || APOL1 G1/G2 risk alleles (sub-Saharan African ancestry) || Explains disproportionate FSGS burden in Black patients; also linked to HIVAN and hypertensive nephrosclerosis
|-
| '''Virus-associated''' || HIV (HIVAN), parvovirus B19, CMV, EBV || HIVAN: collapsing variant; almost exclusively in Black patients; responds to antiretroviral therapy
|}

===Histologic variants (prognostic significance)===
*'''NOS (not otherwise specified):''' most common; intermediate prognosis
*'''Tip lesion:''' best prognosis; most responsive to steroids
*'''Collapsing:''' worst prognosis; associated with HIVAN, severe hypertension, rapid progression to ESKD; massive proteinuria; steroid-resistant
*'''Cellular:''' intermediate prognosis
*'''Perihilar:''' associated with adaptive/secondary FSGS

==Clinical features==
===Nephrotic syndrome (>70% of primary FSGS)===
*'''Edema:''' generalized or dependent; may develop over weeks or have '''abrupt onset with 15-20 lb weight gain'''<ref name="Medscape_FSGS">Focal Segmental Glomerulosclerosis Clinical Presentation. ''Medscape''. 2024.</ref>
**Children: typically begins with '''periorbital/facial swelling''' → progresses to generalized anasarca
**Adults: dependent edema (legs, sacrum); periorbital
*'''Foamy urine''' (proteinuria)
*'''Fatigue, anorexia'''
*'''Ascites, pleural effusions''' (from third-spacing; pericardial effusion is rare)
*Onset frequently follows an '''upper respiratory tract infection'''
*'''Hypertension''' — may be '''severe''' (diastolic >120 mmHg), especially in Black patients with renal impairment<ref name="StatPearls"/>

===Subnephrotic presentation (~30%)===
*Incidental proteinuria found on routine urinalysis
*Microscopic hematuria (occasionally)
*Mild hypertension
*Slowly progressive renal insufficiency

===EM-relevant complications of nephrotic syndrome===
These are the reasons FSGS patients present to the ED:

====Thromboembolism====
*Nephrotic syndrome is a '''hypercoagulable state''' — urinary loss of antithrombin III, protein C, protein S; elevated fibrinogen, factor V, factor VIII; platelet hyperaggregability<ref name="Complications">Complications of nephrotic syndrome. ''Korean J Pediatr''. 2011;54(8):322-328. PMC3212701.</ref>
*Risk: '''deep venous thrombosis, pulmonary embolism, renal vein thrombosis, cerebral sinus thrombosis'''
*VTE incidence ~1-5% in adults (higher in membranous nephropathy); risk is highest in the '''first 6 months'''
*'''Sudden gross hematuria or acute flank pain + acute renal failure''' → suspect '''renal vein thrombosis'''
*'''Acute dyspnea + pleuritic chest pain''' → suspect '''pulmonary embolism'''
*Children: arterial thrombosis (cerebrovascular) can also occur

====Infection====
*'''Immunodeficiency''' from urinary loss of immunoglobulins (especially IgG) and complement proteins
*Immunosuppressive therapy further increases risk
*'''Most common infections:''' pneumonia, sepsis/bacteremia, cellulitis, '''spontaneous bacterial peritonitis (SBP)''', UTI<ref name="Complications"/>
*'''SBP in nephrotic syndrome:''' any child with nephrotic syndrome + fever + abdominal pain + ascites should have '''diagnostic paracentesis''' — ''Streptococcus pneumoniae'' is the most common causative organism; ''E. coli'' and gram-negatives also seen
*Steroid therapy may '''mask typical signs of infection''' — maintain a high index of suspicion

====Hypovolemic crisis====
*Severe hypoalbuminemia (albumin <1.5 g/dL) → decreased oncotic pressure → intravascular volume depletion
*'''Abdominal pain, vomiting, diarrhea, tachycardia, cool extremities, delayed capillary refill, oliguria''' → '''hypotension''' (a late sign)<ref name="Complications"/>
*Can be precipitated by aggressive diuresis or intercurrent illness
*'''Risk of AKI from prerenal azotemia'''

====Acute kidney injury====
*Multifactorial: hypovolemia, sepsis, nephrotoxic medications, renal vein thrombosis, or disease progression
*AKI complicating NS has increased 158% over the past decade in pediatric hospitalizations<ref name="AKI_NS">Rheault MN, et al. Increasing frequency of AKI amongst children hospitalized with nephrotic syndrome. ''Pediatr Nephrol''. 2014;29(1):139-147. PMC6556228.</ref>

====Severe/malignant hypertension====
*May present with hypertensive emergency: headache, visual changes, encephalopathy, seizures

==Differential diagnosis==
===Nephrotic syndrome (other causes)===
*'''Minimal change disease (MCD):''' most common cause in children; clinically indistinguishable from FSGS without biopsy; steroid-responsive; excellent prognosis (distinguishing MCD from FSGS on biopsy is critical because management and prognosis differ)
*'''Membranous nephropathy:''' most common in white adults; strongly associated with renal vein thrombosis; may be secondary to malignancy, hepatitis B, SLE
*'''Diabetic nephropathy:''' most common secondary cause of nephrotic syndrome overall
*'''Lupus nephritis''' ([[SLE]])
*'''Amyloidosis'''
*'''IgA nephropathy''' (nephrotic presentation less common)
*'''HIV-associated nephropathy (HIVAN):''' collapsing FSGS variant; suspect in any HIV-positive patient with nephrotic syndrome

===Generalized edema (non-renal causes to exclude)===
*'''Heart failure''' (elevated JVP, S3 gallop, pulmonary edema)
*'''Cirrhosis/hepatic failure''' (spider angiomata, ascites, jaundice, coagulopathy)
*'''Protein-losing enteropathy'''
*'''Severe malnutrition'''

==Evaluation==
===ED workup===
*'''Urinalysis with microscopy:'''
**'''Heavy proteinuria''' (3+ or 4+ on dipstick)
**Hyaline or broad waxy casts; '''RBC casts are generally absent''' (their presence suggests nephritic syndrome/glomerulonephritis instead)
**Oval fat bodies ("Maltese cross" under polarized light) — pathognomonic for nephrotic-range proteinuria
*'''Spot urine protein:creatinine ratio:''' >3.5 mg/mg indicates nephrotic-range proteinuria (faster than 24-hour collection)
*'''Serum albumin:''' <3.0 g/dL (often <2.0 g/dL in active disease)
*'''BMP/CMP:''' creatinine (renal function), electrolytes, calcium (low from hypoalbuminemia — correct for albumin)
*'''Lipid panel:''' hyperlipidemia (elevated total cholesterol, LDL, triglycerides) — characteristic of nephrotic syndrome
*'''CBC:''' evaluate for infection; anemia (may occur from transferrin loss)
*'''Coagulation studies:''' PT/INR, fibrinogen (if thrombosis suspected)
*'''Blood glucose:''' rule out diabetic nephropathy as underlying cause

===Directed testing based on presentation===
*'''Suspected thromboembolism:''' D-dimer, CT pulmonary angiography (PE), Doppler ultrasound of extremities (DVT), renal vein Doppler (renal vein thrombosis)
*'''Suspected SBP:''' diagnostic paracentesis (cell count, Gram stain, culture, protein, albumin)
*'''Suspected infection:''' blood cultures, urine culture, chest X-ray
*'''New diagnosis workup''' (arrange via nephrology; not all ED tests):
**Complement levels (C3, C4) — normal in FSGS (low in SLE, MPGN, post-infectious GN)
**ANA, anti-dsDNA (lupus)
**Hepatitis B and C serologies
**HIV testing
**Serum free light chains, SPEP/UPEP (amyloidosis, myeloma)
**'''Renal biopsy:''' definitive diagnosis; arranged by nephrology

==Management==
===ED management of nephrotic syndrome complications===

====Edema management====
*'''Salt restriction''' (education; not acute ED intervention)
*'''Loop diuretics:''' furosemide 1-2 mg/kg IV (children) or 20-80 mg IV (adults)
**'''Caution:''' excessive diuresis can precipitate hypovolemic crisis and AKI — monitor volume status carefully
**Diuretic resistance is common in severe hypoalbuminemia (furosemide is protein-bound and may not reach tubular lumen effectively)
*'''IV albumin 25% (0.5-1 g/kg) followed immediately by IV furosemide:''' for '''severe/refractory edema''' or clinical hypovolemia
**Albumin temporarily raises oncotic pressure, mobilizes edema fluid into intravascular space, and enhances diuretic delivery to the kidney
**'''Monitor closely for pulmonary edema''' — albumin infusion can cause fluid overload if the patient is not truly volume-depleted
*'''Do NOT give albumin without concurrent diuresis''' unless treating confirmed hypovolemia — it will redistribute into the extravascular space and worsen edema

====Thromboembolism====
*'''Anticoagulation:''' heparin (UFH or LMWH) followed by warfarin or DOAC per VTE protocols
*'''Thrombolysis or thrombectomy:''' consider for massive PE or limb-threatening DVT per standard protocols
*Renal vein thrombosis: anticoagulation; rarely requires intervention

====Infection / SBP====
*'''Empiric antibiotics:''' broad-spectrum pending cultures
*'''SBP:''' cefotaxime or ceftriaxone (covers ''S. pneumoniae'' and gram-negatives); adjust based on culture
*'''Diagnostic paracentesis''' in any nephrotic patient with ascites + fever or abdominal pain — do not wait for imaging

====Hypovolemic crisis====
*'''IV normal saline 20 mL/kg bolus''' if hemodynamically compromised
*'''IV albumin 25% (1 g/kg over 3-5 hours)''' for severe hypovolemia with albumin <1.5 g/dL
*Monitor blood pressure closely; avoid fluid overload

====Hypertensive emergency====
*Manage per standard [[Hypertensive emergency]] protocols
*ACE inhibitors/ARBs are first-line for chronic BP control AND reduce proteinuria (but avoid in AKI with hyperkalemia)

===Disease-specific treatment (not typically initiated in ED)===
*'''Primary FSGS:''' corticosteroids (prednisone 1 mg/kg/day for 16+ weeks in adults); calcineurin inhibitors (tacrolimus, cyclosporine) for steroid-resistant or intolerant; mycophenolate mofetil; rituximab
*'''Secondary FSGS:''' treat underlying cause (antiretroviral therapy for HIV, weight loss for obesity, stop offending drug); ACE inhibitor/ARB for proteinuria reduction
*'''Genetic FSGS:''' does NOT respond to immunosuppression; ACE inhibitor/ARB and supportive care
*All patients: '''ACE inhibitor or ARB''' (reduces proteinuria independent of blood pressure), '''statins''' (for hyperlipidemia), '''sodium restriction'''

==Disposition==
*'''Admit:'''
**Severe/symptomatic edema unresponsive to oral diuretics
**Thromboembolism (PE, DVT, renal vein thrombosis, cerebral sinus thrombosis)
**Suspected or confirmed SBP or sepsis
**Hypovolemic crisis with hemodynamic instability
**AKI (rising creatinine, oliguria)
**Hypertensive emergency
**New diagnosis with severe nephrotic syndrome requiring urgent nephrology evaluation
*'''Discharge with close follow-up:'''
**Known FSGS patient with stable mild-moderate edema exacerbation responsive to oral diuretics
**No signs of infection, thrombosis, or AKI
**Stable renal function
**Ensure nephrology follow-up within 24-72 hours
*'''Always refer to nephrology''' — FSGS requires biopsy for diagnosis and ongoing specialist management; the EM physician's role is to manage complications and ensure timely referral
*'''Counsel patients on:'''
**Sodium restriction
**'''Signs of thromboembolism''' (leg swelling, dyspnea, chest pain) — seek immediate care
**'''Signs of infection''' (fever, abdominal pain) — low threshold to return
**Medication compliance (steroids, immunosuppressants, ACE inhibitors)
**'''Pneumococcal vaccination''' (if not already received — nephrotic patients are at high risk for pneumococcal infection)

==See Also==
*[[Nephrotic syndrome]]
*[[Nephritic syndrome]]
*[[Acute kidney injury]]
*[[Pulmonary embolism]]
*[[Deep venous thrombosis]]
*[[Spontaneous bacterial peritonitis]]
*[[Hypertensive emergency]]
*[[HIV]]

==External Links==
*[https://www.ncbi.nlm.nih.gov/books/NBK532272/ StatPearls — Focal Segmental Glomerulosclerosis]
*[https://journals.lww.com/cjasn/fulltext/2017/03000/focal_segmental_glomerulosclerosis.18.aspx CJASN — Focal Segmental Glomerulosclerosis (Rosenberg & Kopp, 2017)]
*[https://emedicine.medscape.com/article/245915-overview Medscape — Focal Segmental Glomerulosclerosis]
*[https://www.msdmanuals.com/professional/genitourinary-disorders/glomerular-disorders/focal-segmental-glomerulosclerosis MSD Manual — Focal Segmental Glomerulosclerosis]
*[https://www.kidney.org/kidney-topics/focal-segmental-glomerulosclerosis-fsgs NKF — Focal Segmental Glomerulosclerosis]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC3212701/ Korean J Pediatr — Complications of nephrotic syndrome (2011)]

==References==
<references/>

[[Category:Renal]]

← Older revision		Revision as of 09:36, 22 March 2026
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	==Clinical features==		==Clinical features==
	===Nephrotic syndrome (>70% of primary FSGS)===		===Nephrotic syndrome (>70% of primary FSGS)===
	* Edema: generalized or dependent; may develop over weeks or have ~~'''~~abrupt onset with 15-20 lb weight gain~~'''~~<ref name="Medscape_FSGS">Focal Segmental Glomerulosclerosis Clinical Presentation. ''Medscape''. 2024.</ref>		* Edema: generalized or dependent; may develop over weeks or have abrupt onset with 15-20 lb weight gain<ref name="Medscape_FSGS">Focal Segmental Glomerulosclerosis Clinical Presentation. ''Medscape''. 2024.</ref>
	**Children: typically begins with ~~'''~~periorbital/facial swelling~~'''~~ → progresses to generalized anasarca		**Children: typically begins with periorbital/facial swelling → progresses to generalized anasarca
	**Adults: dependent edema (legs, sacrum); periorbital		**Adults: dependent edema (legs, sacrum); periorbital
	* Foamy urine (proteinuria)		* Foamy urine (proteinuria)
	* Fatigue, anorexia		* Fatigue, anorexia
	* Ascites, pleural effusions (from third-spacing; pericardial effusion is rare)		* Ascites, pleural effusions (from third-spacing; pericardial effusion is rare)
	*Onset frequently follows an ~~'''~~upper respiratory tract infection~~'''~~		*Onset frequently follows an upper respiratory tract infection
	* Hypertension — may be '''severe''' (diastolic >120 mmHg), especially in Black patients with renal impairment<ref name="StatPearls"/>		* Hypertension — may be '''severe''' (diastolic >120 mmHg), especially in Black patients with renal impairment<ref name="StatPearls"/>

Line 53:		Line 53:
	====Thromboembolism====		====Thromboembolism====
	*Nephrotic syndrome is a '''hypercoagulable state''' — urinary loss of antithrombin III, protein C, protein S; elevated fibrinogen, factor V, factor VIII; platelet hyperaggregability<ref name="Complications">Complications of nephrotic syndrome. ''Korean J Pediatr''. 2011;54(8):322-328. PMC3212701.</ref>		*Nephrotic syndrome is a '''hypercoagulable state''' — urinary loss of antithrombin III, protein C, protein S; elevated fibrinogen, factor V, factor VIII; platelet hyperaggregability<ref name="Complications">Complications of nephrotic syndrome. ''Korean J Pediatr''. 2011;54(8):322-328. PMC3212701.</ref>
	*Risk: ~~'''~~deep venous thrombosis, pulmonary embolism, renal vein thrombosis, cerebral sinus thrombosis~~'''~~		*Risk: deep venous thrombosis, pulmonary embolism, renal vein thrombosis, cerebral sinus thrombosis
	*VTE incidence ~1-5% in adults (higher in membranous nephropathy); risk is highest in the ~~'''~~first 6 months~~'''~~		*VTE incidence ~1-5% in adults (higher in membranous nephropathy); risk is highest in the first 6 months
	* Sudden gross hematuria or acute flank pain + acute renal failure → suspect ~~'''~~renal vein thrombosis~~'''~~		* Sudden gross hematuria or acute flank pain + acute renal failure → suspect renal vein thrombosis
	* Acute dyspnea + pleuritic chest pain → suspect ~~'''~~pulmonary embolism~~'''~~		* Acute dyspnea + pleuritic chest pain → suspect pulmonary embolism
	*Children: arterial thrombosis (cerebrovascular) can also occur		*Children: arterial thrombosis (cerebrovascular) can also occur

Line 62:		Line 62:
	* Immunodeficiency from urinary loss of immunoglobulins (especially IgG) and complement proteins		* Immunodeficiency from urinary loss of immunoglobulins (especially IgG) and complement proteins
	*Immunosuppressive therapy further increases risk		*Immunosuppressive therapy further increases risk
	* Most common infections: pneumonia, sepsis/bacteremia, cellulitis, ~~'''~~spontaneous bacterial peritonitis (SBP)~~'''~~, UTI<ref name="Complications"/>		* Most common infections: pneumonia, sepsis/bacteremia, cellulitis, spontaneous bacterial peritonitis (SBP), UTI<ref name="Complications"/>
	* SBP in nephrotic syndrome: any child with nephrotic syndrome + fever + abdominal pain + ascites should have ~~'''~~diagnostic paracentesis~~'''~~ — ''Streptococcus pneumoniae'' is the most common causative organism; ''E. coli'' and gram-negatives also seen		* SBP in nephrotic syndrome: any child with nephrotic syndrome + fever + abdominal pain + ascites should have diagnostic paracentesis — ''Streptococcus pneumoniae'' is the most common causative organism; ''E. coli'' and gram-negatives also seen
	*Steroid therapy may ~~'''~~mask typical signs of infection~~'''~~ — maintain a high index of suspicion		*Steroid therapy may mask typical signs of infection — maintain a high index of suspicion

	====Hypovolemic crisis====		====Hypovolemic crisis====
	*Severe hypoalbuminemia (albumin <1.5 g/dL) → decreased oncotic pressure → intravascular volume depletion		*Severe hypoalbuminemia (albumin <1.5 g/dL) → decreased oncotic pressure → intravascular volume depletion
	*Abdominal pain, vomiting, diarrhea, tachycardia, cool extremities, delayed capillary refill, oliguria → ~~'''~~hypotension~~'''~~ (a late sign)<ref name="Complications"/>		*Abdominal pain, vomiting, diarrhea, tachycardia, cool extremities, delayed capillary refill, oliguria → hypotension (a late sign)<ref name="Complications"/>
	*Can be precipitated by aggressive diuresis or intercurrent illness		*Can be precipitated by aggressive diuresis or intercurrent illness
	* Risk of AKI from prerenal azotemia		* Risk of AKI from prerenal azotemia
Line 102:		Line 102:
	* Urinalysis with microscopy:		* Urinalysis with microscopy:
	** Heavy proteinuria (3+ or 4+ on dipstick)		** Heavy proteinuria (3+ or 4+ on dipstick)
	**Hyaline or broad waxy casts; ~~'''~~RBC casts are generally absent~~'''~~ (their presence suggests nephritic syndrome/glomerulonephritis instead)		**Hyaline or broad waxy casts; RBC casts are generally absent (their presence suggests nephritic syndrome/glomerulonephritis instead)
	**Oval fat bodies ("Maltese cross" under polarized light) — pathognomonic for nephrotic-range proteinuria		**Oval fat bodies ("Maltese cross" under polarized light) — pathognomonic for nephrotic-range proteinuria
	* Spot urine protein:creatinine ratio: >3.5 mg/mg indicates nephrotic-range proteinuria (faster than 24-hour collection)		* Spot urine protein:creatinine ratio: >3.5 mg/mg indicates nephrotic-range proteinuria (faster than 24-hour collection)
Line 134:		Line 134:
	* IV albumin 25% (0.5-1 g/kg) followed immediately by IV furosemide: for '''severe/refractory edema''' or clinical hypovolemia		* IV albumin 25% (0.5-1 g/kg) followed immediately by IV furosemide: for '''severe/refractory edema''' or clinical hypovolemia
	**Albumin temporarily raises oncotic pressure, mobilizes edema fluid into intravascular space, and enhances diuretic delivery to the kidney		**Albumin temporarily raises oncotic pressure, mobilizes edema fluid into intravascular space, and enhances diuretic delivery to the kidney
	**~~'''~~Monitor closely for pulmonary edema~~'''~~ — albumin infusion can cause fluid overload if the patient is not truly volume-depleted		**Monitor closely for pulmonary edema — albumin infusion can cause fluid overload if the patient is not truly volume-depleted
	*'''Do NOT give albumin without concurrent diuresis''' unless treating confirmed hypovolemia — it will redistribute into the extravascular space and worsen edema		*'''Do NOT give albumin without concurrent diuresis''' unless treating confirmed hypovolemia — it will redistribute into the extravascular space and worsen edema

Line 179:		Line 179:
	* Counsel patients on:		* Counsel patients on:
	**Sodium restriction		**Sodium restriction
	**~~'''~~Signs of thromboembolism~~'''~~ (leg swelling, dyspnea, chest pain) — seek immediate care		**Signs of thromboembolism (leg swelling, dyspnea, chest pain) — seek immediate care
	**~~'''~~Signs of infection~~'''~~ (fever, abdominal pain) — low threshold to return		**Signs of infection (fever, abdominal pain) — low threshold to return
	**Medication compliance (steroids, immunosuppressants, ACE inhibitors)		**Medication compliance (steroids, immunosuppressants, ACE inhibitors)
	**~~'''~~Pneumococcal vaccination~~'''~~ (if not already received — nephrotic patients are at high risk for pneumococcal infection)		**Pneumococcal vaccination (if not already received — nephrotic patients are at high risk for pneumococcal infection)

	==See Also==		==See Also==