Nephrolog

Goodpasture’s disease is the most aggressive and rapidly progressive glomerulonephritis
encountered in clinical practice. Crescentic nephritis may be accompanied by lifethreatening
pulmonary hemorrhage.. Treatment with cyclophosphamide, steroids, and plasma exchange can arrest the
disease, but renal damage may be irrecoverabl
. In small-vessel vasculitis, the mainstay of therapy consists of corticosteroids and
cyclophosphamide.. In antineutrophil cytoplasmic autoantibody (ANCA) vasculitis, plasma exchange is
presently recommended in addition to corticosteroids and cyclophosphamide for
patients presenting with advanced renal failure and/or pulmonary hemorrhage.. A high rate of venous thromboembolism has been reported in ANCA vasculitis, with
about 10% of patients developing symptomatic events.


 

How to differentialte acute from Chronic renal failure?

In terms of history, onemust determine whether previous serum creatinines are available or if thereis any history of any systemic diseases that may be associated with renalinvolvement. Often, one must take the time to call otherphysicians or hospitals to get old creatinine values.

When it seems that one isdealing with acute renal failure then there needs to be an assessment forprerenal, renal or post-renal causes.

On physical examination, oneshould look for evidence of a pre-renal cause of renalinsufficiency. Hypovolemia would be suggested byfeatures of decreased extracellular fluid volume such as a low JVP, drymucous membranes or postural tachycardia or hypotension.Pre-renal disease can also be due to conditions such as congestiveheart failure or cirrhosis, so one should also perform a careful cardiacexam and look for stigmata of chronic liver disease.Post-renal failure can be seen in bladder outlet obstruction, so onecould feel for a palpable bladder. Intrinsic renaldisease can develop acutely due to systemic disease with renal involvement.One can look for features of some of these systemic conditions which mightinclude rashes, active joints, alopecia, oral/nasal ulcers, peripheralneuropathy, or a murmur from endocarditis.

In terms of lab data,urinalysis is critical. One may see casts that willhelpful in terms of diagnosis: RBC casts for glomerulonephritis, WBC castsin acute interstitial nephritis and heme granular casts in acute tubularnecrosis. In chronic renal disease, one may see waxy orbroad casts.

Chronic renal failure may alsobe associated with anemia, metabolic acidosis, hypocalcemia andhyperphosphatemia. These may not be entirely reliable,however, as anemia can develop acutely in patients with conditions such aslupus or vasculitis, and hypocalcemia/hyperphosphatemia can be seen inconditions such as tumour lysis syndrome.

On ultrasonography, smallkidneys with cortical echogenicity would suggest kidney disease ischronic. If kidney size is preserved this might suggestacute renal failure, though some diseases of the kidney are associated withpreservation of renal size (examples include diabetic nephropathy andamyloidosis).

Proteinurea: Normal/Abnormal

A 70 kg male performs a 24hour urine collection. The lab report reveals: volume 2.5 L, creatinine 34mmol, protein 240 mg. Do you think this patient has abnormal proteinexcretion? Why?

Answer

To determine adequacy of a 24hour urine collection, one must look at the total amount of creatinineexcreted in the collection period.

Males should excrete 200umol/kg of creatinine per 24 hours and females should excrete 150umol/kg/24 hours.

This patient should haveproduced 70 kg x 200 umol/kg = 14 mmol of creatinine in the 24 hourcollection. Since his collection had 34 mmol ofcreatinine, this represents an overcollection.Therefore, the protein measured is an overestimate of his true 24hour protein excretion. One could estimate that his trueprotein excretion rate would be closer to (14/34) X 240 mg = 99 mg per day,which would fall within the normal range.

Hypocomplementnemia

Question 21
Name 6 diseases that affectthe kidney that are associated with hypocomplementemia.

Answer

Hypocomplementemia in glomerulonephritis is most often due to increased complement consumption. In these cases, immune deposits cause complement consumption at a greater rate than they can be synthesized. Other less common causes of hypocomplementemia are hereditary complement deficiency and the presence of circulating factors that promote complement activation.

Hypocomplementemia can occur with the following conditions: lupus nephritis, subacute bacterial endocarditis, membranoproliferative glomerulonephritis (MPGN), post-streptococcal glomerulonephritis, cryoglobulinemic glomerulonephritis, atheroembolic renal disease, or hemolytic uremic syndrome/thromboticthrombocytopenia purpura.

Pulmonary hypertension in maintenance hemodialysis patients and factors leads to it

ABSTRACT

The aim of this study was to evaluate the prevalence of primary pulmonary hypertension (PH) among Hemodialysis patients and search for possible leading factors. The prevalence of PH was prospectively estimated by Doppler echocardiogram on maintenance hemodialysis patients on the day post dialysis. PH (> 30 mm Hg) was found in 41.3% patients . The hemoglobin and bicarbonate levels were significantly lower in the PH subgroup. 

                

Objective: To determine the prevalence of pulmonary hypertension among chronic hemodialysis patients and the factors leading to pulmonary hypertension.

Material and Methods:

Study design: Cross sectional

Setting: Department of nephrology, Sindh Institute of Urology and Transplantation.

Duration of study: From 19, September 2011 to 19 March, 2012.

Subjects and Methods: 179 patients were included who fulfilled the inclusion criteria after taking the informed consent. SPSS version 17 was used to  analyze the data.

Results:

We studied 179 patients ( males were 115(63.7% and females were  65(36.3%) .The mean±SD of age and duration of HD was (33.8±11.9 years and 23.88±22.13 months). All the them had A-V fistula constructed over therir arms. Out of 179 patients, pulmonary hypertension was found in 74( 41.3%) patients. Frequencies and percentage of the factors which led to pulmonary hypertension were studied, in which  Low  Hemoglobin ( <10 mg/dl) was seen in 70(94.6%): Low bicarbonate(< 24 mEque/L) was found in 71(95.94%):  Low serum albumin(3.4mg/dl)  was seen in 55 ( 74.32%)and  high Ca×P  product was obsereved in 14 (18.91%) patients.

Conclusion :

We found there is  substantial numbers (41.3%) of the  patients on maintenance Hemodialysis(HD) who developed Pulmonary Hypertension. This adds more suffering to these patients who are already attached with  high morbidity . By  timely identifying the factors which leads to this PH, we can take measures to correct them  and reduce the morbidity and mortality related to PH in maintenance HD patients.

Key words:

End stage renal disease, Arterio-venous Fistula, Haemodialysis, Pulmonary hupertension.

CONTRAST NEPHROPATHY

Increased in serum creatinine level is usually wiht 48 to 72 hours.

Rise of creatinine is 0.5 or more than that to base line.

More susciptible group: Advance age; diabetes; cardiac failure; liver failure; multiple myeloma.

Drugs avoided are: NSAIDS; ACE i; Diuretics.

Main stay of treatment : Hydration, Hydration and hyderation .

CONTRAST NEPHROPATHY

Contrast-induced nephropathy, a well-recognized complication of procedures and imaging studies requiring the use of iodinated contrast medium, is linked to increased morbidity. Although a variety of definitions exist, it is generally defined as an increase in serum creatinine level greater than or equal to 0.5 mg/dL or an increase in creatinine level greater than or equal to 25%. Deterioration in renal function is usually identified within 48 to 72 hours after exposure to contrast medium and may occasionally be irreversible. Patients of advanced age and those with diabetes, heart failure, liver failure, existing renal disease, or multiple myeloma are at increased risk. Agents with potential to impair renal response, such as angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, diuretic agents, and nonsteroidal anti-inflammatory drugs, should be withdrawn around the time of the procedure if possible. High contrast medium osmolality and large volumes of contrast medium have been implicated and are generally avoided. Multiple prophylactic measures involving the use of antioxidants and hydration protocols continue to be studied. Periprocedural intravenous hydration has proven to be superior to oral hydration. Although volume expansion with a sodium bicarbonate–based infusion was advantageous in prior trials, recent studies have shown it to have no benefit over sodium chloride and, according to some reports, to potentially add harm in subpopulations.Orally administered acetylcysteine acting as a scavenger of oxygen-derived free radicals has been found to add benefit, although this incremental benefit is modest when 24-hour hydration protocols are in place (and in several trials no benefit has been evident).Despite somewhat ambiguous or conflicting data, it is reasonable to use oral N-acetylcysteine in view of its low cost and minimal adverse effect profile. Aminophylline and ascorbic acid have also been studied without conclusive evidence of benefit.

Clinical Pearl

Periprocedural intravenous volume expansion has been demonstrated to reduce the incidence of contrast-induced nephropathy. The addition of N-acetylcysteine to prophylactic protocols may confer a modest additional benefit.