Chronic Kidney Disease for the Generalist


Protect those nephrons!  From AMR this week, a handy primer on CKD for your continuity clinic.  

When do your patients have CKD? Decline in GFR for >3 months PLUS Evidence of Kidney Disease (evidenced by one of the following)

  • ›Albuminuria
  • ›Urine sediment abnormalities
  • ›Electrolyte and other abnormalities due to tubular disorders
  • ›Abnormalities detected by histology
  • ›Structural abnormalities detected by imaging
  • ›History of kidney transplantation

Figure out what caused it: 75% are HTN and/or Diabetes

  • Glomerular disease
  • Obstructive uropathy
  • Vascular diseases
  • Hepatorenal/cardiorenal syndromes
  • Congenital disease: PKD

Do the workup:

  • GET THE UA  Active sediment/proteinuria vs a bland UA will be a major branch point in your evaluation, so you have to get a UA.  Spot urine protein and creatinine are also useful.
  • US Looking for cystic kidneys, hydronephrosis, asymmetry, or even symmetric evidence of “medical renal disease” is useful.
  • Based on historical clues, you can also check: HIV, hepatitis serologies, SPEP/UPEP, ANA, ANCAs

Stage it: based on GFR. VGFR- MDRD and CKD-EPI are most commonly used formulas. Here’s a handy calculator that gives you both, plus the stage.

Stage Description GFR
1 Kidney damage with nl GFR >90
2 Kidney damage with increased GFR 89-60
3a Moderately decreased GFR 59-45
3b 44-30
4 Severely decreased GFR 29-15
5 Kidney failure <14 or on dialysis


Call for Backup: Nephrology Referral

  • You don’t know why the patient has kidney disease
  • It is progressing quickly (loss of 50% of their GFR within one year)
  • Nephrosis: Lots of proteinuria (>3g/day)
  • Nephritis: active urine sediment with blood, protein, casts
  • Dialysis planning: sometime during stage3b is probably ideal, certainly by the time patient has GFR <30
    • Mortality benefit for patients that see nephrology earlier.

OK, now what?  Manage it:

  • Fix reversible causes: remove nephrotoxins, relieve obstruction, treat CHF/Cirrhosis/HIV/Hepatitis
  • Slow progression
    • HTN: JNC8 guidelines recommend goal 140/90
    • DM: ACCORD trial showed benefit with treatment to HbA1c <7.5
    • Add an ACE-inhibitor or ARB if there is proteinuria
  • Aggressive cardiovascular risk reduction (Cardiovascular disease is going to kill these patients before the renal disease does- see graph below)
  • Deal with the complications

CV mortality in CKD

Sarnak M J et al. Circulation. 2003;108:2154-2169

What Complications?

  • Hyperkalemia: Lasix helps
  • Anemia: Replace Iron, consider EPO if Hgb <10
  • Acidosis: consider when serum bicarb <22
  • Volume Overload: Lasix helps
  • Mineral Bone Disease: replace Vitamin D, bind PO4

Great posts by our own Dr.Centor on CKD here (don’t miss the comments) and here.

2012 KDIGO Guidelines for the evaluation and management of CKD.



Well, I was publicly called out this week to do a post, so I better deliver. Thanks much for the suggestion,  my goal is always to provide interesting, relevent content that helps you out in clinic.  Remember that you can search the whole blog with the search box, tags, or use the big categories at the top of the page. Archives are there to help you!

Anyway… on to vertigo!

Vertigo is a sensation of movement without moving.  If you’ve done this…

or this…or this…

then you know vertigo.

A big branch point in the differential diagnosis is Central vs Peripheral causes. Central causes are the “scarier” ones: brainstem or cerebellar stroke/TIA or MS. Peripheral causes are the ones we are more comfortable diagnosing and treating: BPPV, Meniere’s diease, vestibular neuritis, acoustic neuroma. Migrainous vertigo can walk the line between central and peripheral, and have features of both.

Most vertigo has some postural instability associated, and it often feels worse to move the head in the midst of an attack. Specific, predictable maneuvers (like rolling over in bed) that precipitate vertigo should make you think of BPPV. Most patients with peripheral causes of vertigo should be able to walk. When the postural instability is so severe that they can’t walk, that points toward a central cause.

Vertigo doesn’t last forever. Even with permanent damage to the vestibular system, the body compensates and the vertigo subsides. However, the time course can help you with the diagnosis: BPPV usually is short-lived– a minute or less, while migrainous vertigo can last minutes to hours.  Vestibular neuritis, brainstem infarction and MS can produce vertigo that is severe and lasts for days.

Nystagmus is often found with vertigo. Central causes can have nystagmus in any direction, while peripheral causes will only have horizontal nystagmus. Nystagmus that reverse direction when the patient looks from right to left suggests a central cause.

Apart from the Romberg and nystagmus, an otherwise normal neurologic exam suggests a peripheral cause.  If your patient has weakness, cerebellar signs, or abnormal reflexes, be worried about those central causes.  Interestingly, hearing loss or tinnitus does suggest a peripheral cause, most commonly Meniere’s disease or acoustic neuroma.

Of course, there are some specific maneuvers that can help you out. The Dix Hallpike maneuver is most helpful if your patient is not symptomatic when you examine them. If you can elicit the vertigo and/or nystagmus with the maneuver, it is suggestive of BPPV.  My favorite video demonstration of Dix-Hallpike is here.

There is also the Head Thrust Maneuver. This is useful for diagnosing vestibular neuritis as compared to a central vertigo. The concept is that the patient focuses on a distant object, and tries to maintain focus while the examiner abruptly turns the patient’s head about 15 degrees. A normal response is to keep the eyes fixed on the object.  Patients with cerebellar lesions have a normal response. The abnormal response is for the eyes to deviate, toward the lesion, and then slowly return to the object. Peripheral causes of vertigo, like vestibular neuritis, tend to result in an abnormal head thrust response.

Up To Date has a great table to help differentiate the common and concerning causes of vertigo. It is so good, I’ve just reproduced it here for you.  Another great resource for dizziness in general is this AAFP article (if you don’t have institutional access, Am Fam Physician. 2010 Aug 15;82(4):361-368).
Time course Suggestive clinical setting Characteristics of nystagmus• Associated neurologic symptoms Auditory symptoms Other diagnostic features
Benign paroxysmal positional vertigo Recurrent, brief (seconds) Predictable head movements or positions precipitate symptoms Peripheral characteristics None None Dix-Hallpike maneuver shows characteristic findings
Vestibular neuritis Single episode, acute onset, lasts days Viral syndrome may accompany or precede vertigo Peripheral characteristics Falls toward side of lesion, no brainstem symptoms Usually none Head thrust test usually abnormal
Meniere disease Recurrent episodes, last minutes to several hours Spontaneous onset Peripheral characteristics None Episodes may be preceded by ear fullness/pain, accompanied by vertigo, unilateral hearing loss, tinnitus Audiometry shows unilateral low frequency sensorineural hearing loss
Migrainous vertigo Recurrent episodes, last several minutes to hours History of migraine Central or peripheral characteristics may be present Migraine headache and/or other migrainous symptoms accompanying or following vertigo Usually none Between episodes, tests are usually normal
Vertebrobasilar TIA Single or recurrent episodes lasting several minutes to hours Older patient, vascular risk factors, and or cervical trauma Central characteristics Usually other brainstem symptoms Usually none MRI w/DWI may demonstrate vascular lesion
Brainstem infarction Sudden onset, persistent symptoms over days to weeks As above Central characteristics Usually other brainstem symptoms, especially lateral medullary signs Usually none; an exception is anterior inferior cerebellar artery syndrome MRI will demonstrate lesion
Cerebellar infarction or hemorrhage Sudden onset, persistent symptoms over days to weeks Older patient, vascular risk factors, especially hypertension Central characteristics Gait impairment is prominent. Headache, limb dysmetria, dysphagia may occur. None Urgent MRI, CT will demonstrate lesion
* Other diagnoses described in text “Pathophysiology and differential diagnosis of vertigo”.
• Peripheral characteristics of nystagmus: horizontal or horizontal-torsional; suppresses with visual fixation, does not change direction with gaze. Central characteristics of nystagmus: may be horizontal, torsional, or vertical, does not suppress with visual fixation, may change direction with gaze.