Nephrology

Hyponatremia

Hypervolemic Hypo-Natremia

• Causes:
  • CHF
  • Cirrhosis
  • Nephrotic Syndrome

Euvolemic Hyponatremia

• Causes:
  • Compulsive H2O drinking (Psychogenic polydipsia)

HypOvolemic Hypo-Natremia

• Causes:
  • Adrenal Insufficiency
  • Diuretics  (urine sodium elevated)
  • GI loss of fluids (vomiting, diarrhea)
  • Renal
  • Skin loss of fluids(Burns, Sweating)
• Management:
  • Correct the underlying cause and replace it with normal (isotonic) saline. Remember to check serum sodium frequently.

Hyper-Kalemia (K+)

• Diagnosis:
  • First peaked T-waves occur, then loss of the P-wave, and then the widened QRS complex occurs.
    
• Management:
  • Moderate HyperKalemia with no EKG abnormalities:
    
    • 1 – Insulin and glucose intravenously.
    • 2 – Bicarbonate to shift K+ into the cell when acidosis is the cause of the K+ or there is rhabdomyolysis, hemolysis, or another reason to alkalinize the urine.
    • 3 – Kayexalate (K+-binding resin) is administered orally to remove K+ from the body. This takes several hours.
      
      
  • Severe HyperKalemia with EKG abnormalities:
    
    • 1 – Administer Ca++ gluconate IV to protect the heart.
    • 2 – Follow with insulin and glucose IV.
    • 3 – Conclude with Kayexalate.
      
      
  • Bicarbonate MOA to lower K+:
    
    • When alkalosis pulls H+ out of cells, another cation must go in to maintain electrical neutrality. As H+ ions come out of cells, K+ goes in.

HypO-Kalemia

• EKG
  • Show “Uwaves,” which have an extra wave after the T-wave indicative of Purkinje fiber repolarization.
• Management:
  • IV K+ replacement must be slow so as not to cause an arrhythmia with overly rapid administration.
  • Avoid:
    
  • Glucose-containing fluids in cases of HYPO-K+. They will increase insulin release and worsen hypokalemia.

Hyper-Magnesimia

• Presentation:
  • muscular weakness and loss of deep tendon reflexes.
• Management:
  • 1. Restricting intake
  • 2. Saline administration to provoke diuresis
  • 3. Occasionally dialysis

HypO-Magnesimia

• Presentation:
  • HYPO-Ca++ and cardiac arrhythmias
•  Causes:
  • – Loop diuretics
  • – Alcohol withdrawal, starvation
  • – Drugs: Gentamicin, amphotericin, diuretics, Cisplatin
  • – Parathyroid surgery
  • – Pancreatitis

Hyperphosphatemia

• Leads to deposition of Ca in BV > calcified arteries > calciphylaxis
  
• Need to remove phosphate from diet and treat with phosphorous binders

Acid-Base Disorders

Metabolic Acidosis

Metabolic Alkalosis

Respiratory Acidosis

Respiratory Alkalosis

Hypertension

Primary Hypertension

• BP measurement procedures:
  • White coat HTN: 15-20% =lifestyle changes
    
  • Masked HTP 10-15% =tretment
    
  • Use home BP/24hour BP for diagnosis of hypertension
• When to start high BP treatment:
  • 120/80 start non-pharmacological therapy
    
  • >140/90 start treatment or >130/80 with CVD or great live time risk
• Lifestyle modifications for HTN (5):
  • Weight reduction
    
  • DASH eating plan
    
  • Na+reduction
    
  • Exercise
    
  • Moderation of alcohol
• BP target for HTN patients:
  • 130/80
• Medication for HTN:
  
  1. NO DM or CKD
     
     1. Nonblack: ACEI, ARB, or CCB
        
     2. Black: Thiazide or CCB
        
  2. DM/CKD
     1. ACEI or ARB

Secondary hypertension

• Presentation:
  • 1. Young-onset
    
  • 2. Sudden onset
    
  • 3. Refractory hypertension (drug-resistant)
    
  • 4. Malignant hypertension (super high BP, with quick onset
• Endocrine Causes:
  • Primary Aldosteronism
    
  • Causing Syndrome
    
  • Pheochromocytoma
    
  • Renin Secreting Tumors
    
  • Hyperthyroidism

Primary Aldosterone

• Presentation:
  • Primary: High Aldo but low Renin
    
  • -unregulated secretion of aldosterone by the adrenal gland (adenoma, adrenal hyperplasia, Conn’s syndrome)
    
  • -New refractory HTN
    
  • -Hypokalemic
    
  • -metabolic alkalosis
• Diagnosis:
  • Aldosterone/Renin ratio 20:1
    
  • -confirm after salt loading
    
  • CT of adrenal
    
  • Adrenal vein sampling: determines unilateral or bilateral
    
• Management:
  • Adrenal Hyperplasia: Medical management, blocks aldosterone receptor (Aldactone or eplerenone)
    
  • Adrenal Adenoma: surgical removal if unilateral, medical if bilateral

Cushing Syndrome

• Presentation:
  • -HTN, buffalo hump, moon fancies, hirsutism, easy brusing
• Path:
  • Glucocorticoids (cortisol) excess from adrenal gland due to overproduction of ACTH by pituitary adenoma -> unchecked activation of mineralocorticoid receptor
• Diagnosis:
  • absence of cortisol suppression following dexamethasone administration
• Treatment:
  • remove adenoma

Pheochromocytoma

• Presentation:
  • Headaches, sweating, HTN, tachycardia caused by sudden release of catecholamines
• Path:
  • Rare neuroendocrine tumor that produces norepinephrine, epinephrine, and dopamine
    
  • 90% in adrenal glands and benign
    
  • Can occur on their own or part of a syndrome
• Diagnosis:
  • Biochemical testing
    
  • -plasma free catecholamine metabolites
    
  • Ct or MRI of the abdomen
    
• Treatment:
  • Surgical removal of the tumor

Hyperthyroidism

• Elevated TH stimulates sympathetic nervous system and HTN

Renovascular Hypertension

• Features:
  • Most common cause of secondary hypertension, 10-15% of refractory hypertension
    
  • Unilateral or Bilateral
    
  • Episodic malignant hypertension
    
  • Flash pulmonary edema
    
  • Significant rise in creatinine when started on RAAS blocking in bilateral
    
• Causes:
  
  • 1. Fibromuscular dysplasia
    
    • Non-atherosclerotic
      
    • A string of beads on Radiographic of renal artery
      
    • -congested/twisty renal artery
      
    • Commonly seen in young females
  • 2. Atherosclerosis
    • Most common cause of renovascular hypertension
      
    • Generally patients greater than 50 with known atherosclerosis
      
    • Typically occurs in the optimum or proximal portion of renal artery
      
    • -closer to the aorta
• Unilateral vs. Bilateral:
  • Unilateral:
    • -constant elevation of renin/angiotensin/aldosterone out runs the normal kidney
    • compensation
    • -normal kidney keeps volume low
    • -secondary aldosterone
    • -treat with hormone blockers
  • Bilateral:
    • -high BP maintained by retention of salt and water
    • -treat with diuretics
    • -can have significant rise in creatinine with RAAS blocker
• Diagnosis:
  • Blood test: elevated renin and aldosterone
    
  • Imaging: ultrasound, CT, MRI
    
  • Percutaneous catheter placement to measure Intravascular pressure
    
• Treatment:
  • RAAS, CCB, Diuretics
    
  • Fibromuscular: balloon dilation
    
  • Atherosclerotic: only use balloon dilation with stents in extreme cases

Renal Parenchymal Hypertension

• Presentation:
  • Renal Failure Hypertension
    
  • Elevated Na, increase in RAAS activity, overactivity of a sympathetic nervous system
    
• Treatment:
  
  • -low Na diet
    
  • -diuretics
    
  • -RAAS blockers (ACE-I, Angio REceptor blockers)
    
  • -Beta-Blockers
    
  • -Dialysis

Sleep Apnea

• HTN occurs due to activation of the sympathetic nervous system and RAAS
  
• Suspect if snore, or ease, thick neck, or daytime sleepiness
  
• Treat with CPAP: continuous positive airway pressure

Coarctation of the aorta

• Congenital narrowing of the aorta, on the downturn
  
• Hypertension in upper limbs, with reduced BP in lower limbs
  
• Delayer femoral pulses
  
• Kids diagnosed with imaging, surgical treatment

Kidney Disorders

Acute Interstitial Nephritis

• Inflammatory attack of tubules
  
• Skin rash, arthralgias, or arthritis
  
• Rising BUN and Creat
  
• Urine: WBC WBC casts, granular casts, eosinophils
  
• CBC: elevated WBC/eosinophils
  
• *Confirmatory diag=renal biopsy
  
• Most common cause: medications
  
• Treat with steroids

Chronic Interstitial Nephritis

• Caused by: medications, heavy metals, autoimmune, etc
  
• ALWAYS presents as a Progressive Kidney Failure Syndrome > Chronic Kidney Disease
  
• Slow rises of BUN/Creat

Acute tubular Injury/Necrosis

1. Ischemic: Spotty thought out
   1. Causes: blood loss, hypotension, septic shock, surgery
   2. Symptoms: Oliguria, Low BP, shock
2. Toxic: whites out the PCT and DLH
   1. Causes: drugs, antibiotics, chemo
   2. Symptoms: non-specific, can have normal urine
3. Inflammatory
4. Obstruction

   **Hyperkalemia, Rising BUN/Creat
   Tubular casts and Granular casts

Nephritic Syndromes

• Path:
  • INFLAMMATION of the kidney
    
  • Systemic disease-causing -itis
    
• Urine:
  
  • RBC in urine
    
  • Low protein
    
  • WBC
    
  • Low GFR
    
  • Hypertension
    
• Causes:
  • Alpert Syndrome, post-infection, IgA nephropathy, membranoproliferative GN, Lupus,
  • Rapidly progressive necrotizing glomerulonephritis
• Serum Complement Levels:
  • LOW C3 & Normal C4
    
    • -PIGN
      
    • -MPGN
      
  • Low C3 & C4
    • -Lupus
      
    • -Cryoglobulinemia
  • Normal C3&C4
    
    • -ANCA
      
    • -ANTI GBM
      
    • -IgA/HSP
      
    • -Alpert/TBM
• Treatment:
  • 1. Immunosuppression: HUGE steroids
    
    • -select immune suppression based on the underlying disease
      
  • 2. HTN Management
    
  • 3. Plasmapheresis in select cases (Goodpasture’s)

Rapidly progressive glomerulonephritis

• Acute Crescentic Necrotizing GN: SICK. Often have pulmonary and renal symptoms
  
• Causes:
  
  • 1. Immune complex
    • -lupus, IgA Nephropathy, post-infectious GN, cryoglobulinemic GN, Membranoproliferative
      
  • 2. Pauci-immune (no immune complexes, intrinsic inflammation)
    
  • 3. Anti-glomerular basement membrane (Goodpasture’s)

Crescent Glomerulonephritis

• Necrosis of capillaries
  
• Fibrin released into Bowman’s space attracts macrophages > macrophages engulf fibrin > epithelioid cell
  
• Give steroids

Nephrotic Syndromes

• Presentation:
  • high PROTEIN >150g in urine
    
  • Hyperlipidemia
    
  • Not as sick as Nephritic
    
• Urine: 
  • Foamy urine
    
  • Edema
    
  • Can have stable GFR
• Complications:
  • Hypoalbuminemia
    
  • Protein malnutrition
    
  • Hyperlipidemia
    
  • Hypovolemia
    
  • AKI
    
  • Thromboembolism
    
  • Infection

Minimal change disease

• Most common cause of nephrotic syndrome in children, biopsy in adult
  
• Complete loss of Podocytes
  
• Sudden onset
  
• Drug-induced
  
• Steroid receptive
  
• Increased risk of VTE

Focal Segmental Glomerulosclerosis

• Primary Congenital vs. Secondary HTN obesity ect.
  
• Podocytes loss
  
• Sudden onset
  
• Treat with steroids

Membranous Nephropathy

• Primary (immune), Secondary (drugs, malignancy, viral)
  
• Immune deposits in the basement membrane
  
• Treat based on protein levels with cyclophosphamide and steroids

Primary Amyloidosis

• Amyloid with mesangial deposits in Glomerular basement membrane
  
• Treatment based on systemic disease
  
• Extremely poor prognosis

Diabetic Nephropathy

• Always progressive without hypoalbuminemia
  
• Decline in GFR related to proteinuria
  
• Treat with ACEI/HTN and glucose control

Renal Tubular Acidosis (RTA)

Type I Distal RTA

• H is not excreted
• Urine anion gap is +
• Alkaline urine
• Calcium phosphate and struvite kidney stones
• Hypercalciuria
• Hypokalemia
• Sjogren syndrome and rheumatoid arthritis
• Rickets
• Treated with Sodium bicarbonate

Type II Proximal RTA

• Bicarbonate is not reabsorbed (FE is high)
  
• Acidic urine
  
• Hypokalemia
  
• Fanconi syndrome
  
• Multiple myeloma
  
• Acetazolamide
• Treated with Sodium bicarbonate

Type IV RTA

• Low aldosterone/low renin
  
• Hyperkalemia
  
• Acidic urine
  
• Addison’s disease
• Potassium inhibits Ammonia formation in type IV RTA
• Type IV RTA is treated with Mineralocorticoid (fludrocortisone)

Proteinuria

Isolated/Benign Proteinuria

• Post-exercise-induced proteinuria
  
• Orthostatic Proteinuria
  
• Younger patients
  
• Not well understood

Tubular proteinuria

• The proximal tubule isn’t reabsorbing spill protein
  
• In Chronic and acute tubule-interstitial disease
  
• Will also see glycosuria and phosphaturia
  
• Drug-induced, systemic disease, infections

Overflow proteinuria

• Overproduction of protein from systemic disease that overwhelms proximal tubule

Non-Renal Proteinuria

• Inflammation anywhere in the GU tract
  
• Infection, Nephrolithiasis
  
• Minimal protein

Chronic Kidney Disease

• Definition:
  • GFR <60cc/min or structural/functional abnormalities and a normal GFR
    
  • Normal GFR >90cc/min
• Staging System:
  • 0: >90 increased risk
    
  • 1: >90 kidney damage
  • 2: 60-89 kidney damage with mild -GFR
    
  • 3: 30-59 moderate -GF
    
  • 4: 15-29 severe -GFR
    
  • 5: <15 or dialysis Kidney Failure

Dialysis

• Patient break down:
  • 50% diabetic
    
  • 27% hypertension
    
  • 13% glomerulonephritis
    
  • 10% other (cancer, GI issues, infection, genetic disease)
• Initiation of Dialysis:
  • Remove nitrogenous waste and replenish bicarb
    
  • URGENT:
    
    • -severe acidosis, electrolyte abnormalities, medication overdose, volume overload
• Hemodialysis Complications:
  • Usually feel good at first then cause hypotension
    
  • -nausea, cramping, infection, anemia, renal osteodystrophy
• Peritoneal Dialysis:
  • Exchange of solutes takes place across the peritoneal membrane
    
  • **Enhanced quality of life
    
    • LOWER infections rates
      
    • Less dietary restrictions
      
    • Gentler process
      
    • Done at home at night
      
    • Can work

GFR measurement

• Insulin clearance = gold standard
  
• 24-hour urine: use in extreme age, body size, vegetarian diet, or weird conditions
  
• Prediction equations=what people actually use
  
• -CKD-EPI, MDRD, Cockcroft-Gault

CKD and Anemia

• Low GFR > Hemoglobin falls
  
• -EPO deficiency, uremic toxins, shortened RBC life span, blood loss, hyperparathyroidism
  
• Treatment:
  • with iron and B12
    
  • -exogenous EPO in severe cases because of stroke risk

Renal Osteodystrophy

• 1. Osteitis fibrosa-high bone turnover from hyperparathyroidism hormone
  
• 2. Osteomalacia- defective mineralization and increased matric synthesis
  
• 3. A dynamic Bone disease- low bone turnover from over suppressed PTH

Secondary Hyperparathyroidism

• Decreased in functional renal mass > inhibition of Vit D processing
  
• Treat with Vit D

Simple Cysts

• Benign, acquired with age
  
• Rare under the age of 50
  
• Rare cause of flank pain or hypertension

Tuberous sclerosis

• Type fo polycystic kidney disease
  
• Angiofibromas on face
  
• Seizures, intellectual disabilities
  
• Respiratory compromise
  
• Recurrent Hematuria
  
• Increased risk of renal cell carcinoma

PKD (polycystic kidney disease)

• Ciliopathy
  
• Rental degeneration, loss of smell, obesity, diabetes, liver fibrosis
  
• ADPKD is most common gene mutation

ADPKD

• Autosomal dominant polycystic kidney disease
  
• Slow gradual bilateral kidney enlargement and loss of kidney function
  
• Pain, kidney stones
  
• Hypertension, hepatic cysts, diverticulosis
  
• PKD1 mutation: 85%
  
  • -more severe and faster than PKD2
    
• PKD 2 mutation
  
  • -fewer cysts, slower progression, less severe

ARPKD (Autosomal Recessive Polycystic Kidney Disease)

• 10% of PKD
  
• PKHD1 mutation
  
• Presents in childhood and is severe

Kidney Stones

• Causes:
  • Hot climate
    
  • Disease of affluence- high salt and meat diets. Low in fluids and potassium, calcium, and veggies
    
  • Increased with age, obesity, diabetes
    
  • More common in whites
    
  • Prevalence increasing in general and in women
    
  • Likely to reoccur
• Kidney Stone Types:
  • 1. Calcium oxalate
    
  • 2. Mixed
    
  • 3. Calcium apatite
    
  • 4. Uric acid
    
  • Uric acid more common after 55
    
  • CaOX more common in summer
• Stone Types and Bowel Disease:
  • Small Bowel Disease: Calcium Oxalate
    
  • Colon Resection: Urate Stones
    
  • Colectomy: Uric Acid Stones
    
  • Ileostomy: Calcium oxalate or Uric Acid
    
  • Gastric Bypass: fulminant Hyperoxaluria
• Risk Factors:
  • Hypercalciuria
    
  • Low urine volume
    
  • Low urine pH
• Treatment:
  • Renal colic, Hematuria, no fever
    
  • Image in fever developers or symptoms worsen
    
  • Consider medical expulsion therapy if stable
    
  • Drugs to promote urethral relaxation
    
  • Less the 3mm should be able to pee it out

Chronic Kidney Stone

• 1. Increase fluid intake
• 2. Increase calcium intake
• 3. Long-acting Thiazide to decrease hypercalciuria
  • -mild volume depletion > increase sodium in PCT > increase Ca intake in PCT
• 4. Potassium citrate if uric acid stones
  • -chelates calcium increases urine pH
• 5. Allopurinol
  • -decrease uric level if citrate fails

Cystine Stones

• Defect in PCT reabsorption of cysteine, causing stones
  
• Autosomal recessive
  
• Hexagonal crystals in acidic urine
  
• treat with urinary alkalinization, citrate therapy

Medullary Sponge Kidney

• Malformation of terminal collecting ducts makes it easier for things to calcify in abnormal ducts
  
• Medullary cysts
  
• Stones, Hematuria, recurrent UTI

Labs

Dipstick Urinalysis

• High sensitivity for albumin, will not detect non-albumin protein
  
• False-positive: alkaline or concentrated urine
  
• False Negative: Acidic or dilute urine