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Section 1 Acute Renal Injury in setting of surgery and post surgery patient.

Causes of Increased BUN: GI bleeds hypercatabolic state i.e. in the setting of malignancy, TPN, burn victims, patients on steroids

Systematic approach:

1)pre-renal

-Hypovolemia: n/v, hemorrhage, burn victims, hypotension may present as SBP of 120 in setting of pre-existing HTN resulting in decreased renal perfusion

2)renal

-rhabdomyolysis d/t anesthetics or malpositioning during surgery

-MCC AKI = ATN: supportive care with slow recovery phase, tubules regenerate prognosis depends on pre-existing kidney disease in the setting of CKD may lead to dialysis dependence

-MCC AIN= medications i.e. NSAIDs, beta-lactam antibiotics; type IV hypersensitivity rxn, present with macular rash, peripheral eosinophilia, urine eosinophils, early recognition important because removal of drug is treatment and delay may lead to permanent injury with tubular atrophy; urine eosinophils may also be seen with prostatitis, cholesterol emboli

-Pyuria with negative urine culture: TIN d/t autoimmune dz (sarcoidosis, SLE), renal tuberculosis order urine AFB, cholesterol emboli

-cholesterol emboli: occurs 1-3 weeks following procedure look for livedo reticularis, emboli phenomenom in digits

-contrast nephropathy occurs hours to days with rapid rise in serum creatinine

Diabetes insipidius side effect, Li has narrow therapeutic window, watch out for toxicity.

-Li toxicity: concentration defects such as nephrogenic DI (patient develops polydipsia)

-types of casts: granular (ATN), RBC/acanthoycytes (GN), WBC casts (AIN, pyelo), fatty (high protein nephrotic syndrome, maltese cross), crystals (acyclovir, uric acid)

-oxalate stones seen in RXY gastric bypass surgery, IBD, short gut syndrome, primary hyperparathyroidism (poss d/t malignancy may need CT with IV contrast)

3)post-renal: BPH, neurogenic bladder, order PVR generally greater than 150 consistent with post-renal aetiology of AKI

Case 2-Nephrotic Syndrome

A 40yo male has come to your office with complaint of swelling of his body over the past several months. He states that approximately 3 months prior to admission he had fallen off his bicycle and bruised his right leg. He noted swelling in the leg at that time and soon thereafter noted both his legs had become swollen. over the past several months he noticed this swelling had increased over his entire body. He reports a 20lb weight gain over that period of time.

 

Discussion Points:

What are the possible etiologies of this patient’s leg swelling? Edema can occur from multiple sources of organ dysfunction; namely, Liver, heart and kidney. Signs of liver cirrhosis include edema, telangiectasias, asterixis, hematemesis, right upper quadrant pain, and caput medusae. Renal pathology can present with edema, flank pain or tenderness, oliguria and abnormal Urinalysis. Cardiac failure can produce edema as well as elevated JVP and shortness of breath.

He has no history of heart disease and denies PND, DOE, or orthopnea, He has no history of liver disease and denies a history of IV drug use. He was never told of any problems with his kidney as an adult or a child. His urinary frequency is unchanged over the past two months.

Discussion points: This history allows us to rule out certain etiologies as to the edema. Cardiac origin is less likely due to no history of heart disease, no orthopnea, and no history of IV drug use which is a risk factor to endocarditis. Liver disease is unlikely also because of lack of IV drug use (viral hepatitis). He also does not present with any other symptoms that would point towards liver failure. At this point it is appropriate to look for signs for renal injury which include swollen eyelids.

 

On physical exam, he appears grossly edematous and puffy. His BMP is 145/98, P-92, RR-16, T-98.6. The patient’s skin shows no signs of jaundice or telangiectasias. He has no signs of palmar erythema. His face shows swollen eyelids but sclera are not icteric. Examination of the neck shows no signs of jugular venous distention and no thyromegaly. His lung exams are clear to auscultation and percussion with the exception of decreased breath sounds and dullness to percussion in the bases. Cardiac exam revealed a non-displaced PMI. Normal S1 and S2 without murmurs, rubs, S3 or S4. Abdominal exams showed the liver to be approximately 9cm in size. No splenomegaly was appreciated. There were findings of shifting dullness to percussion of the abdomen. In the periphery the patient had 4+ pitting edema to the level of the sacrum and throughout both legs. The patient had no signs of gynecomastia, testicular atrophy or parotid swelling. the patient’s neurological exam was normal.

Discussion points:  The pack of jaundice, telangiectasias and palmar erythema further make liver disease less likely. splenomegaly would point toward liver cirrhosis which in this case there is no splenomegaly. His eyelid edema is more indicative of renal dysfunction. Physical exam is also negative for CHF. To pursue a case of renal injury, the next best labs to obtain would be a UA, 24hr urine sample and CMP.

A urinalysis revealed 4+ proteinuria with a microscopic exam that revealed several waxy casts, oval fat vodie, no cellular casts, 1 PRC and 1WBC per high-powered field. Electrolytes included a BUN of 20, a creatinine of 1.3, other electrolytes, glucose, calcium and phosphorus were normal. A 24hr urine collection showed 12 grams of protein and creatinine clearance of 72ml/min. LFTs were no0rmal, as was prothrombin time. The patient’s albumin was 1.9, and serum cholesterol was 670. Chest x-rays revealed bilateral pleural effusions without signs of pulmonary venous engorgement or abnormalities in the cardiac silhouette.

Discussion point: The UA shows proteinuria with waxy casts. Protein in the urine is indicative of nephrotic syndrome. Twenty-four hour urine collection is a quick, simple diagnostic test that helps to diagnose problems with the kidneys. It is commonly performed to determine how much creatinine clears through the kidneys, but may also be used to measure protein, hormones, minerals, and other chemical compounds. Creatinine clearance testing provides information about kidney function. A measure greater than 3g correlates with nephrotic syndrome. With nephrotic syndrome as the diagnosis, we consider further laboratory testing.

Laboratory tests were sent for antinuclear antibodies, serum complement, and fasting blood sugar which all were normal. A VDRL and Hepatitis B and C serologies were also negative.

Discussion point:

There are several conditions to consider in nephrotic syndrome:

MCD (Minimal change disease) – More common in children. good prognosis and responds well to steroid therapy.

FSGN (Focal Segmental Glomerulosclerosis) – Most common in adults. prognosis is not as good as MCD.

MGN (Membranous glomerulonephritis) – autoimmune response results in inflammation and “leaky kidneys.”

RPGN (Rapidly progressive glomerulonephritis) – characterized by a rapid decrease in rate and a crescent moon shape appearance on microscopy.

 

Other kidney disorders/pathologies include the ANCA disorders:

Goodpasture syndrome – antibodies against the basement membrane in the glomerulous and in the lungs resulting in renal injury and lung disease.

Churg-strauss aka eosinophilic granulomatosis with polyangiitis – also autoimmune but presents with elevated eosinophils and patients often present with allergic rhinitis or asthma.

Granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis – also autoimmune attack of the small and medium vessels leading to kidney injury. It is associated with concurrent sinusitis.

The patient is informed of his diagnosis of nephrotic syndrome and the potential benefits and risk of a kidney biopsy in looking for the ideology of this problem. He consented and the procedure is done without complications. The results of the biopsy showed evidence of membranous Glomerulonephritis.

Discussion points:

It is important to weigh the risks and benefits of biopsy. Contraindications to biopsy include bleeding or coagulopathy disorders, stents, and other comorbidities that make biopsy a high risk procedure.
The patient is informed of his prognosis and the diagnosis of membranous GN. He is started on a course of corticosteroid therapy in conjunction with cyclophosphamide. He will be followed up closely for side effects of the medication as well as the effect on the patient’s renal function as well as level or proteinuria.

 

Dr. Ben-Zur is a cardiologist who sees patients from Burbank, Encino, Sun Valley, Beverly Hills, Brentwood, Marina del Rey, Inglewood, El Segundo, Manhattan Beach, Redondo Beach, Torrance, Hollywood, Bel Air, Malibu, Calabasas, Saratoga Hills, Agoura hills, Thousand Oaks, Sherman Oaks, Studio City, Simi Valley, West Hills, Reseda, and Oak Park. He sees patients with all types of heart disease, including atrial fibrillation, a-fib, AF, sick sinus syndrome, av block, heart block, arrythmias, ischemia, congestive heart failure. He places pacemakers, defibrillators, implantable cardiac defibrillators. Bi-ventricular pacing.

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