Nephrology

·         HENOCH-SCHÖNLEIN PURPURA (HSP):

mnemonic: AGAR

Abdominal pain

Glomerulonephritis

Arthralgia

Rash

·         Purpura (livedo reticularis) after a coronary angiogram: think CHOLESTEROL ATHEROEMBOLIC DISEASE

·         Purpura (livedo reticularis) + hepatitis B + abdominal pain after meals + footdrop +HTN: think POLYARTERITIS NODOSA

·         THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP):

mnemonic: FAT RN

Pentad:

1. Fever

2. Anemia, microangiopathic hemolytic (+) schistocytes

3. Thrombocytopenia

4. Renal abnormalities

5. Neurologic abnormalities (confusion, aphasia,headache, coma, seizures)

·         HEMOLYTIC UREMIC SYNDROME (HUS):

mnemonic: RAT

Renal failure

Anemia, microangiopathic hemolytic

Thrombocytopenia

The FAT RN has TTP and her HUS has a RAT

TTP and HUS both have

(1) Normal coagulation tests (normal PT/PTT)

(2) Elevated LDH

HUS is similar to TTP, except that it only affects the RENAL system

·         URINARY CASTS-REVIEW

Normal RBCS excretion == 2 millions RBCs/day

Hematuria == 2--5 RBCs Per HPF.

GRANULAR CAST === Significant renal disease (ARF)

Hyaline cast === most frequently (M.C.)==normal/mild renal disease.

Epithelial cast ==== disease affecting tubules/ ATN.

Broadcast / Waxy cast === chronic renal disease/CRF, Malignant HTN, Diabetic nephropathy.

RBCs/Dysmorfic(>5%) RBCs cast == Glomerular injury (kidney) / PSGN.

WBCS cast == Pyelonephritis

Lipid cast == Nephrotic synd.

·         Hyperglycemia lowers the plasma sodium concentration; in the absence of insulin, glucose is an effective osmole that attracts water from cells and thereby dilutes extracellular sodium. Therefore, the blood glucose level should always be examined when a low plasma sodium concentration is being evaluated.

·         In SIADH, urinary sodium matches intake; as the urine is usually concentrated, the urinary sodium concentration exceeds 40 mEq/L unless dietary sodium intake is very low. The urinary osmolality also is inappropriately increased. BUN and serum uric acid are usually low in patients with SIADH. In patients with asymptomatic hyponatremia secondary to SIADH, the treatment of choice is fluid restriction. Administration of normal saline in patients with SIADH can worsen the hyponatremia. Thiazides block the reabsorption of sodium and chloride in the distal tubule and can lead to severe hyponatremia.

·         Creatinine clearance (CCr) can be measured by 24-hour collection of urine, or it can be estimated through use of a formula that involves the patient's age, ideal body weight (IBW), and plasma creatinine (Cr): CCr = (140 – age) × (IBW in kg)/(72 × Cr). In females, the results are multiplied by a correction factor of 0.85.

·         CKD is defined as either kidney damage or a GFR of less than 60 ml/min/1.73 m2 for longer than 3 months. The MDRD and Cockcroft-Gault equations provide useful estimates of GFR in adults.

·         Potassium balance is generally maintained within normal limits until the GFR falls to less than 10 ml/min. This balance is achieved by an increased potassium excretion rate per remaining nephron, as well as an increase in extrarenal potassium excretion, primarily effected via the colon. The development of hyperkalemia at higher levels of renal function suggests the presence of tubulointerstitial disease or disturbances in the renin-angiotensin-aldosterone axis.

·         As renal function continues to decline, calcium and phosphorus levels remain within the normal range initially but at the expense of an ever-increasing level of PTH. Critical interventions include keeping phosphate levels down, assuring adequate calcium ingestion, and, if necessary, replacing hydroxylated vitamin D.

·         The extent to which urea clearance leads to underestimations of GFR is similar to the extent to which creatinine clearance leads to overestimations of GFR. Thus, taking the average of urea and creatinine clearance values will give a very accurate estimation of GFR.

·         Aggressive control of hyperglycemia may be more likely to slow progression of renal disease in patients with type 1 diabetes mellitus than in patients with type 2 diabetes mellitus.

·         ANCA–associated glomerulonephritis is not associated with staining for immunoglobulin, complement, or immune deposits.

·         Glucocorticoids represent the key initial medical therapy for patients diagnosed with FSGS.

·         It is estimated that 10% to 40% of patients with nephrotic syndrome will develop arterial or venous thromboembolism. Urinary losses of antithrombin III are thought to contribute to the pathogenesis of this complication.

·         Patients with IgA nephropathy typically present with nephritic-like symptoms that derive from deposition of IgA in the glomeruli. It is the leading cause of glomerulonephritis worldwide. The male-to-female ratio is 3:1. The classic presentation in up to 50% of patients with IgA nephropathy is episodic macroscopic hematuria within 24 hours of a mucosal infection of the upper respiratory tract. The majority of the rest of patients with IgA nephropathy present with persistent asymptomatic microscopic hematuria. This differs from the hematuria of poststreptococcal glomerulonephritis, which is delayed by 2 to 3 weeks following pharyngitis. The macroscopic hematuria usually resolves within days.

·         ACE inhibitors and ARBs should be used cautiously in patients with PAN, because renal involvement may produce a functional equivalent of classic renal artery stenosis.

·         Plasma ADAMTS (a disintegrin and metalloprotease with thrombospondin type 1 motif)  activity must be severely depressed for TTP to develop. The level of ADAMTS-13 plasma activity is modestly depressed in patients with liver disease, disseminated cancer, chronic metabolic and inflammatory conditions, and pregnancy, as well as in newborns. When plasma activity of ADAMTS-13 falls to less than 5% of normal, these large von Willebrand antigens predominate, bind to platelets, and cause aggregation and thrombi in small vessels.

Clopidogrel is a thienopyridine (these agents is to prevent ADP-induced platelet aggregation by irreversibly inhibiting the P2Y12 receptor) antiplatelet agent that is known to be associated with life-threatening hematologic effects, including neutropenia, TTP, and aplastic anemia. The true incidence of TTP associated with thienopyridine use is unknown, but it occurs with both clopidogrel and ticlopidine use. When compared to ticlopidine, TTP associated with clopidogrel use occurs earlier (often within 2 weeks) and tends to be less responsive to therapy with plasmapheresis. In addition, individuals with TTP associated with clopidogrel generally have a higher platelet count and creatinine and their TTP is less likely to be associated with ADAMTS13 deficiency. The mortality of TTP associated with thienopyridines is approximately 25–30%.

·         In patients with Wegener granulomatosis who are in remission, trimethoprim-sulfamethoxazole is used to prevent relapse of disease; it is not used in patients with active disease.

·         Celiac or renal angiographic findings of microaneurysms and irregular, segmental constriction of the larger vessels with tapering and occlusion of smaller intrarenal arteries are diagnostic of classic polyarteritis nodosa.

·         The extent of renal involvement is the most important prognostic factor in Henoch-Schonlein purpura.

·         Two heavy metals—lead and cadmium—clearly produce tubulointerstitial damage.

·         The renal dysfunction has a negative impact on platelet function. Desmopressin appears to help with platelet function. As there is generally an adequate platelet count, platelet transfusion does not have much impact. Vitamin K is used to help reverse problems with the extrinsic clotting cascade.

·         Kidney transplant recipients initially have an increase in mortality, but they have an overall improvement in long-term survival.

·         Antimetabolites, however, such as azathioprine and mycophenolate mofetil, are important in immunosuppressive agents in renal transplantation, because of their lack of nephrotoxicity and because they have little effect on blood pressure.

·         BPH involves prolonged exposure of the prostate gland to androgens. In the prostate, interactions between epithelial and stromal cells and the extracellular matrix, mediated primarily by locally produced (intrinsic) growth factors, appear important. These peptide growth factors, which include fibroblast growth factors, insulinlike growth factors, and epidermal growth factors, are felt to be the local forces that determine prostate growth