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Flashcards in Renal Diseases Deck (118):

In primary care, often have reason to be concerned about the possibility of kidney disease in kids who present with ____ or __ in their urine or with __ or ___ problems

blood or protein in their urine or with hypertension or growth problems


Functions of the kidney

1. Filtration and Elimination of waste products in the form of blood urea nitrogen (BUN), uric acid and creatinine
2. Maintain circulatory volume and acid-base balance
3. Hormonal regulation and Hormonal response
4. Blood pressure regulation


in dehydration/shock situations, the kidney will maintain circulatory volume at the expense of ____, which, along with the lung, maintains the optimum ____

acid-base regulation

pH of our blood.


The kidney is responsible for producing what?

1. renin
2. erythropoietin
3. active form of vitamin D


what is Renin?

a key component in the renin-angiotensin-aldosterone regulation of blood pressure


What is erythropoietin

The hormone which signals the bone marrow to produce red blood cells


How does ADH affect the kidney

increase reabsorption of H20


How does PTH affect the kidney

Increase reabsorption of Ca2+


How does aldosterone affect the kidney

Increase reabsorption of Na+ and excretion of K+

-increases BP


How does ANH,ANP hormone affect the kidney?

Decrease reabsorption of Na+


Describe the renin-angiotensin cascade

Decreased BP--> renin released from kidney--> cleaves angiotensinogen from liver into angiotensin I--> cleaved by ACE from lung into angiotensin II--> vasoconstricts BV and stimulates adrenal cortex to release aldosterone--> increase Na+ and H20 reabsorption = increase BP


Clinical presentation of renal failure

1. AMS
2. N/V
3. malaise
*caused by significant electrolyte imbalances


Presentation of chronic renal insufficiency

1. HTN
2. various lab abnormalities: proteinuria or elevated BUN or Cr
3. growth failure


Causes of pre-renal acute failure

-etiologies which decrease circulating volume:
1. blood loss,
2. dehydration,
3. shock including anaphylaxis, cardiogenic or septic, heart failure)

- or blocked blood flow to the kidneys:
4. renal artery thrombi/masses or
5. trauma


Lab findings with pre-renal failure

1. High BUN and Cr w/ BUN greater than Cr*
2. Low urine Na+**
3. High urine specific gravity*
4. low urine output


Causes of intrinsic renal failure

1. damage to the tubules (shock, toxins)
2. microvascular injury (HUS)
3. glomerular injury (PSGN, HSP, SLE)
4. Interstitial cell injury (Drugs)


Describe the prognosis of intrinsic renal failure

While some intrinsic renal failure is recoverable, some of the causes listed here can result in permanent renal damage and some degree of chronic renal insufficiency/failure


Causes of post renal failure

1. anything that causes obstruction to urine flow such as anatomical abnormalities:
2. UPJ obstruction
3. posterior urethral valves,
4. neurogenic bladder

5. or acquired obstructions:
6. renal stones
7. Foreign body,
8. masses,
9. trauma


in post renal failure, Because the obstruction needs to be bilateral or at the level of the bladder or lower to cause symptoms of acute renal failure, the consequence of ___ is rarely seen

poor urine output


Lab findings associated with intrinsic renal failure

1. High BUN and Cr with Cr greater than BUN*
2. high urine Na+, urine sediment


Lab findings associated with post renal failure

1. high urine Na+
2. low urine specific gravity*


Whatever the cause, as renal function decreases the serum creatinine level will ___.

Ex- a child whose normal Cr is 0.5, who now has a Cr of 2.0, how has their GFR changed?

rise proportionally

-so that for every doubling of serum creatinine, the renal clearance, expressed as glomerular filtration rate (GFR), has been halved.

For example a child whose normal Cr is 0.5, who now has a Cr of 2.0 (doubled twice 0.5 to1, 1 to 2) has decreased their GFR to 25% (halved twice 100%to50%,50%to 25%).


Obvious renal failure does not result until ___% of nephrons are lost in both kidneys (progressively)



End-stage renal disease is defined by

as GFR less than 15% and requires dialysis as well as medications to take the place of hormones the kidney would have produced


What kind fistula is commonly used for hemodialysis and peritoneal dialysis

-hemodialysis: forearm AV fistula

-peritoneal dialysis: peritoneal shunt


causes of chronic renal insufficiency

1. intrinsic ones
2. DM
3. renal scarring from missed urinary malformation
4. PKD


What causes HUS (hemolytic-uremic syndrome)?

E. Coli O:157 bacteria found in fresh vegetables, undercooked hamburger, unpasteurized fruit and milk, petting zoos


Initial illness of HUS presents as

vomiting and bloody diarrhea after ingestion of the bacteria


How does E. Coli O:157 cause HUS?

-This strain of E. Coli carries a Shiga toxin, which targets the endothelial cell layer of blood vessels, which results in cell death and microthrombi. The damaged blood vessels result in shearing forces on the passing RBC’s, resulting in hemolysis.
-The vessel damage occurs in the nephron of the kidney, resulting in kidney damage and possible acute renal failure
-There is additional microvascular bleeding in the skin resulting in a petechial rash


how do HUS damaged cells appear?

"helmet" cells


Work up and treatment of HUS

1. All patients with bloody diarrhea will have a stool culture, but if you suspect exposure to E. Coli O:157, you must specify that on the lab order
2. The treatment of the initial diarrheal illness consists of supportive inpatient care, as antibiotic treatment is associated with an increased likelihood of HUS
3. sometimes requires dialysis and transfusions


Who is most at risk for HUS after E. Coli O:157 diarrhea?

young and elderly


describe the prognosis of HUS

variable w/ some pts dying and others having a complete recovery and some w/ residual renal insufficiency

*most pediatric patients do recover


Presentation of renal tubular acidosis (RTA) in children

1. usually presents as growth failure
2. polyuria
3. episodes of dehydration
4. rickets
5. renal stones


What is Rickets

a bony deformity of the legs, which involves the femur and tibia resulting in patellas that are rotated laterally


Renal rickets, due to RTA, is caused by:

abnormalities of electrolytes including calcium and phosphorous, due to the kidney’s poor ability to control the reabsorption and secretion of electrolytes.

*Renal rickets is so rarely seen in the US that RTA is an important differential to consider here
*caused by nutritional deficiencys in developing countries


What is the difference between Type I and II RTA?

-Type I RTA- there is insufficient secretion of H+ into the urine, again resulting in a metabolic acidosis. As the blood pH drops, hypokalemia can result.
-usually permanent defect

-Type II RTA- the proximal tubule does not resorb bicarbonate ion, resulting in a metabolic acidosis.
- typically outgrown by age 4yr


How do you treat RTA type I and II

1. . Both types can be treated with large amounts of buffer (citrate) to overcome how much they are losing in their urine, and treatment of this disorder is managed by a nephrologist.


From a primary care standpoint, the work-up of a pt w/ growth failure includes:

1. CMP- which will include serum bicarbonate, as well as all electrolytes, BUN and Cr
2. venous blood gas, as the lungs should be increasing CO2 excretion in response to the metabolic acidosis, if the problem is renal in origin.
3. A renal ULTZ looking for renal stones or hydronephrosis


When should you refer a pediatric patient to nephrology with suspected RTA?

Pediatric patients with:
1. metabolic acidosis,
2. elevated BUN/Cr,
3. renal stones

should be referred to nephrology for suspected RTA.


Patients w/ ___ should see a urologist to look for ___


obstructive anomalies


key elements when assessing a patient with red urine

1. history
2. appropriate lab testing


Infants in the first week of life often have ___ in their urine, leading to a brick-red colored urine in their diaper.
-It is concerning to parents, so reassurance is necessary.

urate crystals


what medication can cause red urine?

Pyridium- urinary tract anesthetic


What causes myoglobinuria?

1. severe muscle trauma
2. burns
3. dehydration

**substantial muscle breakdown


____ is toxic to the renal tubules and can result in acute renal failure.


**it is important to watch someone w/ a hx of myoglobinuria


How can you differentiate between and upper (nephron) vs lower tract bleeding?

-dark "cola-colored" urine
+ dip stick
-urine microscopy w/ dysmorphic RBS and RBC casts

-Red or pink urine
+ dip stick
-urine microscopy of WHOLE RBCs w/ NO casts


urine RBC’s ____ is considered clinically insignificant and no work-up is necessary.

less than 5/hpf


When blood is coming from a damaged nephron will have traveled through the glomerulus when it shouldn’t have, it will be ____

dysmorphic or broken


RBC’s will get squished together in the ____ forming a red cell cast, a gelatinous tubule-shaped stack of RBC’s

distal collecting duct


gelatinous tubule-shaped stack of RBC’s

RBC casts


Where can lower tract bleeding come from?

1. renal calycyes
2. ureters
3. bladder
4. urethra

*often caused by UTIs


DDX for red urine

1. infants- urate crystals
2. meds- Pyridium
3. Rhabdomyolysis due to trauma, severe dehydration- myoglobinuria
4. Upper tract (nephron)
5. Lower tract (calcyces, ureters, bladder, urethra)
6. menstruation
7. urine obtained via catheterization
8. hematuria


most common causes of hematuria

1. post-streptococcal glomerulonephritis (PSGN)*
2. IgA nephropathy
3. Henoch-Schonlein Purpura (HSP)*
4. SLE
5. Membranoproliferative Glomerulonephritis (MPGN)

*managed in primary car w/ phone calls to nephrology


Patients diagnosed with HSP only need ___ for signs of hematuria indicating renal involvement

urine monitoring


What renal disease cause hematuria and have a low C3 complement component, and how do they present?

2. SLE
3. MPGN (persistently low)

*present w/ more gross hematuria vs dark urine of most renal diseases w/ hematuria


MPGN is often initially diagnosed as ___ these



How can you differentiate MPGN and PSGN

MPGN will have a persistently low C3 level
-PSGN will return to normal in 4-6 weeks


What should you do in the setting of persistently low C3 levels?

refer to nephrology as these patients will need a renal biopsy to determine if their hematuria is actually MPGN


What is the primary care approach to PGSN

1. manage HTN
2. tx for GAS if ASO/Streptozyme +
3. supportive care/wait for remission


Presentation of PSGN

1. Recent URI
2. sore throat or impetigo
3. may have dark urine,
4. edema
5. HTN
6. proteinuria
7. Age 2-12 y/o


PSGN lab findings

1. ASO + if strep throat
2. Streptozyme + if impetigo
3. low C3


What is the primary care approach to IgA Nephropathy

referral to nephrology


What is the primary care approach to suspected MPGN

referral to nepthrology


What is the primary care approach to HSP

1. supportive care
2. watch for hematuria or abdominal pain
3. watch for GI vasculitis- risk for intussusception
4. involve nephrology if hematuria develops in a pt with HSP


What is the primary care approach to SLE

refer to rheumatology


What is the clinical presentation for IgA nephropathy

1. Male
2. Adolescent
3. Recurrent episodes of bloody urine


What is the clinical presentation for HSP

1. Palpable purpuric rash
2. joint swelling/pain
3. renal/GI vasculitis
4. 3-15 y/o


What is the clinical presentation for SLE

1. hematuria in the setting of recurrent/prolonged fever
2. malar rash
3. arthritic joint sx
4. adolescent


What is the clinical presentation for MPGN

1. Hematuria sometimes w/ proteinuria
2. may look like PSGN
3. child-young adult


What are the lab findings for IgA nephropathy

1. C3 normal


What are the lab findings for HSP

1. high WBC
2. high CRP, ESR
3. normal plt count
4. may have hematuria
5. +/- proteinuria if renal involvement


What are the lab findings for SLE

1. Low C3
2. + ANA
3. + Ab to dsDNA


What are the lab findings for MPGN

1. Persistently low C3


What should you do if want to test for ANA to assess for SLE nephritis?

phone consult w/ pediatric rheumatologist bc ANA are very non-specific and weakly positive ANA's generate a lot of parental anxiety and fill up the schedules of pediatric rheumatologist, and, at the end, often have a neg. work up for SLE


Who should be tested for SLE

those who meet the diagnostic SLE criteria


How should a gross or symptomatic microscopic hematuria guide your work up?

1. hx of trauma--> CT of abdomen and pelvis
2. sx of UTI--> urine culture, abx ,recheck UA after
3. sx of perineal or meatus irritation--> reassurance and supportive care
4. sx of renal/ureteral stones--> imaging (renal u/s, abdominal plain film)
5. sx of glomerular source (proteinuria, or RBC casts)--> check BUN/Cr, electrolytes, CBC, C3, C4, Albumine and consider ASO, streptozyme, ANA testing --> refer to nephrologist


What should you do w/ a pt w/ hematuria with no obvious cause on hx, physical, or urinalysis?

1. urine culture
2. urine calcium/creatinine ratio
3. test parents for hematuria
4. hemoglobin electrophoresis
5. renal u/s


When does protein sometimes spill into the urine

1. activity
2. when glomerular capillary membrane is damaged by disease


what is often used in lieu of the 24hr urine collection used to determine urinary protein lossses

using a single urinalysis and calculating the urine protein/serum creatinine ratio

*In order to use the ratio, both the urine protein and the creatinine must be expressed in mg/dl.


When proteinuria is present with hematuria, consider ___



When proteinuria is present with hypertension, the patient may have ___

significant renal insufficiency


what proteinuria is presetnt w/ edema consider __

nephrotic syndrome or glomerulonephritis


when proteinuria is present with polyuria, consider __

chronic renal insufficiency or urinary tract anomalies.


what is 1+ , 2+, 3+, 4+ urine dipstick mean

trace or neg is normal
1+ = 30mg/dl
2+ = 100mg/dl
3+ = 300 mg/dl
4+ = 1000mg/dl


what is a normal and a nephrotic range of urine protein/creatinine ratio

Normal: less than 0.2

Nephrotic range: over 2.0


These patients do not spill protein until they are more active during the day, so this represents an exaggeration of normal physiology

orthostatic proteinuria


Clinical presentation of orthostatic proteinuria

1. adolescent age
2. Asymptomtatic
3. isolated finding
4. no hematuria
5. normal BP
6. normal anatomy
7. Urine protein/Cr ratio on AM urine slightly higher PM but not nephrotic


Clinical presentation of nephrotic syndrome

1. any age, but more common 2-5y/o
2. edema
3. proteinuria w/ urine protein/Cr ratio in nephrotic range
4. low serum albumin
5. increased lipids
6. increased risk of clotting, infections, and severe edema


Clinical presentation of Minimal change (Nil) Disease

1. less than 6y/o
2. significant periorbital/pretibial edema
3. +/- HTN or ascites
4. proteinuria
5. low serum albumin
6. Cr may be low
7. possible minimal hematuria less than 20-30 RBCs's/hpf


Clinical presentation of Mesangial nephropathy

1. any age
2. proteinuria
3. low serum albumin
4. edema


Clinical presentation of Focal Segmental Glomerulosclerosis (FSGS)

1. less than 6y/o
2. proteinuria
3. low serum albumin
4. high serum creatinine
5. significant hematuria
6. elevated B/P


nephrotic syndrome has an increased risk of what?

clotting, infections, and severe edema


tx of nephrotic syndrome

1. prednisone 2mg/kg/d (max 80) x 6 weeks, then QOD then taper
2. follow pt clinicaly for complications and HTN

*managed in primary care unless the edema is severe, there are complications or an alternative dx is considered, or not improving as expected


tx of minimal change (Nil) disease

prednisone and nephrologist


tx of mesangial nephropathy

prednisone and nephrologist


tx of FSGS

-less responsive to prednisone
-may progress to renal failure


tx of orthostatic proteinuria

1. get f/u first AM urinalysis to verify protienuria
*. It is sometimes prudent to follow the urinalysis a couple of times in the next year, as their initial small proteinuria may progress into proteinuria that needs further workup


What lab should you always get with periorbital swelling



All proteinuria which falls within nephrotic range will also have an associated ____. It may or may not have ___ or __

low serum albumin.

an elevated creatinine or elevated b/p.


Most nephrotic syndrome remits in ___

2-3 weeks


What diseases should be suspected if what was thought to be a nephrotic patient also has or develops hematuria, elevated Cr, or HTN.

1. Minimal change (Nil) disease
2. mesangial nephropathy
3. focal segmental glomerulosclerosis (FSGS)

*involve an nephrologist if these occur


What should you do if you find 1+ or greater proteinuria in a child incidentally?

1. obtain 1st AM void for urine total protein/creatinine ratio and UA w/ microscopic exam
2. if 0.2mg or less of protein per mg creatinie and normal UA --> repeat dipstipstick on first AM void in 1 yr
2. if over 0.2mg protein per me creatinine or abnormal UA--> evaluate fhx, hx of drugs, PE/BP, labs, and other tests--> if normal repeat urine dipstick on at least 2 additional samples
--> if abnormal refer to nephrology


What should you do if renal utlz reveals obstructive uropathy?

referral to urologist NOT nephrologist

*They need to have their obstruction corrected and then if they still have proteinuria, may need to see a nephrologist for management of their possible renal damage.


What is the work up symptomatic proteinuria

if nephrotic syndrome--> tx w/ prednisone and assess respone--> refer to nephrology

if +hematuria glomerulophritic--> see hematuria/GN algorithm


What labs should you obtain if you find 1+ or greater proteinuria in a child incidentally with over 0.2mg protein per me creatinine or abnormal UA

1. creatinine
2. BUN
3. electrolytes
4. cholesterol
5. albumin


for BP
-lower than 90th percentile is: __
-90-95th percentile is: __
-95-99th percentile is: __
-Over 99th is: __

-lower than 90th percentile is: normal
-90-95th percentile is: high
-95-99th percentile is: significant
-Over 99th is: severe


It is important to have __ BP readings on __ separate occasions prior to determining the child is hypertensive, although primary care providers should move forward with an evaluation/management on a child with severe HTN, or evidence of hypertensive emergency with H/A, visual disturbance, seizures, focal neurologic findings, altered mental status or chest pain




Children rarely have essential or primary hypertension unless they are __ and __

obese and over 12y

*always make sure it is the right cuff size and always recheck staff BP


DDX of secondary HTN

1. coarctation of the aorta
2. renal disease (70%)
-Post-streptococcal glomerulonephritis (PSGN)
-renal insufficiency
-+/- minimal change (Nil) disease
-Focal Segmental Glomerulosclerosis
3. hyperthyroidism (rare)
4. pheocromocytoma (rare)


When evaluating pediatric HTN, what hx info is important?

1. PMH for UTIs, prematurity w/ umbilical cath or bronchopulmonary displasia
2. Meds
3. FHx for DM, HTN, cardiac/renal dz, dyslipidemia


When evaluating pediatric HTN, what PE is important?

1. growth: wt and ht failure
2. VS: BP and HR
3. HEENT: papilledema
4. thryoid
5. cardiac/pulses: murmur, edema, brachiofemoral lag
6. abdomen: masses, renal bruit
7. GU: ambiguous genitalia (CAH)
8. skin: dry or sweating
9. Neuro: focal deficits


When evaluating pediatric HTN, what ROS info is important?

1. HEENT: symptoms of OSA
2. renal: gross hematuria, edema, enuresis,
3. cardiac: chest pain, dyspnea, palpitations, claudication,
4. endocrine: sweating, weight loss, diarrhea(hyperthyroid and pheo), weight gain, constipation (hypothyroid),
5. rheumatologic: rash, joint symptoms, persistent/recurrent fever,
6. CNS: H/A, visual changes, gait disturbances


What is the level 1 work up for pediatric HTN

1. electrolytes
2. BUN/Cr
4. thyroid
5. CBC
6. UA + micro
7. renal u/s

* done in primary care


The Level 1 work-up for HTN is done in primary care, looking for evidence of:

1. renal insufficiency,
2. vasculitis/anemia due to renal disease,
3. thyroid disorders
4. renal artery stenosis.

*If the history, PE or labs point toward a disease process listed here, treat or refer as appropriate.


What is the level 2 workup for pediatric HTN?

*sometimes necessary to do in primary care-- but contact a nephrologist for further guidance

1. fasting glucose
2. lipid panel
3. plasma renin activity
4. serum aldosterone and cortisol
5. echo


When do you refer a kid to cardiology for HTN?

1. evidence of aortic coarctation
2. evidence of CHF

**never refer pt to cardiology for HTN of uncertain etiology


What renal disease can cause HTN

1. Post-streptococcal glomerulonephritis (PSGN)
2. renal insufficiency
3. +/- minimal change (Nil) disease
4. Focal Segmental Glomerulosclerosis